Objective: To investigate the sequential mediation effects of pain and activities of daily living (ADLs) on the relationship between multimorbidity and depressive symptoms among middle-aged and older adults in rural China, providing evidence to optimize health management strategies.
Methods: Using four waves of data (2011-2018) from the China Health and Retirement Longitudinal Study (CHARLS), cross-sectional logistic models and panel random-effects models were used to examine the associations and effects of multimorbidity, pain, ADLs, and depression. Structural equation modeling (SEM) combined with the Bootstrap method was applied to analyze the mediation pathways.
Results: A total of 2949 middle-aged and older participants were included in the study. When instrumental activities of dailyliving (IADLs) were used as the mediator, approximately 48.44% of the association between comorbidity and depression was attributable to the mediating path of physical pain and IADLs (0.051, 95% CI: 0.045-0.056). When basic activities of daily living (BADLs) were used as the mediator, approximately 47.91% of the association between comorbidity and depression was attributable to the mediating path of physical pain and BADLs (0.050, 95% CI: 0.045-0.056). The chain mediating pathways involving physical pain and the development of daily living abilities were both statistically significant (0.005, 95% CI: 0.004-0.006).
Conclusion: Multimorbidity directly increases the risk of depression and also exacerbates this risk through pain and subsequent declines in ADLs, either independently or sequentially.
{"title":"[The Association Between Depressive Symptoms and Multimorbidity Among Middle-Aged and Older Adults in Rural China: Sequential Mediation Effects of Pain and Activities of Daily Living].","authors":"Chiyu Li, Hongyu Lai, Jie Pan","doi":"10.12182/20260160508","DOIUrl":"10.12182/20260160508","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the sequential mediation effects of pain and activities of daily living (ADLs) on the relationship between multimorbidity and depressive symptoms among middle-aged and older adults in rural China, providing evidence to optimize health management strategies.</p><p><strong>Methods: </strong>Using four waves of data (2011-2018) from the China Health and Retirement Longitudinal Study (CHARLS), cross-sectional logistic models and panel random-effects models were used to examine the associations and effects of multimorbidity, pain, ADLs, and depression. Structural equation modeling (SEM) combined with the Bootstrap method was applied to analyze the mediation pathways.</p><p><strong>Results: </strong>A total of 2949 middle-aged and older participants were included in the study. When instrumental activities of dailyliving (IADLs) were used as the mediator, approximately 48.44% of the association between comorbidity and depression was attributable to the mediating path of physical pain and IADLs (0.051, 95% CI: 0.045-0.056). When basic activities of daily living (BADLs) were used as the mediator, approximately 47.91% of the association between comorbidity and depression was attributable to the mediating path of physical pain and BADLs (0.050, 95% CI: 0.045-0.056). The chain mediating pathways involving physical pain and the development of daily living abilities were both statistically significant (0.005, 95% CI: 0.004-0.006).</p><p><strong>Conclusion: </strong>Multimorbidity directly increases the risk of depression and also exacerbates this risk through pain and subsequent declines in ADLs, either independently or sequentially.</p>","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"202-208"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12979994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To investigate the association between the expression levels of galectin-9 and sonic hedgehog (SHH) and the risk of occurrence and prognosis in patients with colorectal cancer (CRC).
Methods: A total of 210 patients with CRC treated at Qingdao Traditional Chinese Medicine Hospital between May 2020 and May 2022 were retrospectively included. The expressions of galectin-9 and SHH in tumor tissues were measured. Logistic regression was used to analyze the relationship between galectin-9/SHH expression and CRC risk. Receiver operating characteristic (ROC) curves were plotted to evaluate the predictive value of galectin-9 and SHH for CRC risk and prognosis.
Results: The expression levels of galectin-9 and SHH differed significantly between cancer tissues and adjacent normal tissues (P<0.05). ROC analysis showed that the AUCs for galectin-9 and SHH in evaluating CRC risk were 0.809 (95% CI: 0.751-0.868) and 0.865 (95% CI: 0.817-0.912), respectively. Galectin-9 expression was lower in patients with T3-4 stage, N1-3 stage, M1 stage, or poor differentiation (P<0.05), whereas SHH expression was higher in these patients(P<0.05). Galectin-9 expression was negatively correlated with SHH expression and TNM stage (r=－0.184 and －0.362, respectively; P<0.001). SHH expression was positively correlated with TNM stage (r = 0.407, P< 0.001). Significant differences in galectin-9 and SHH expression were observed between patients with poor prognosis and those with good prognosis (P< 0.05). Logistic regression analysis indicated that T3-4 stage (OR= 4.609, 95% CI: 1.461-14.535), poor differentiation (OR=3.337, 95% CI: 1.297-8.582), and high SHH expression (OR= 2.067, 95% CI: 1.162-3.678) were risk factors for poor prognosis (P< 0.05), while high galectin-9 expression (OR = 0.652, 95% CI: 0.437-0.975) was a protective factor (P< 0.05). The AUCs of galectin-9 and SHH for evaluating CRC prognosis were 0.769 (95% CI: 0.550-0.798) and 0.734 (95% CI: 0.603-0.866), respectively.
Conclusion: Galectin-9 and SHH are lowly and highly expressed, respectively, in CRC. Their expression levels are associated with tumor differentiation, invasion, and metastasis, and hold predictive value for the risk and prognosis of CRC patients.
{"title":"[Role of Galectin-9 and Sonic Hedgehog Expressions in the Early Diagnosis and Prognosis of Colorectal Cancer].","authors":"Qian He, Xin Liu, Tiantian Lin, Xiaonan Dong","doi":"10.12182/20260160603","DOIUrl":"10.12182/20260160603","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the association between the expression levels of galectin-9 and sonic hedgehog (<i>SHH</i>) and the risk of occurrence and prognosis in patients with colorectal cancer (CRC).</p><p><strong>Methods: </strong>A total of 210 patients with CRC treated at Qingdao Traditional Chinese Medicine Hospital between May 2020 and May 2022 were retrospectively included. The expressions of galectin-9 and <i>SHH</i> in tumor tissues were measured. Logistic regression was used to analyze the relationship between galectin-9/<i>SHH</i> expression and CRC risk. Receiver operating characteristic (ROC) curves were plotted to evaluate the predictive value of galectin-9 and <i>SHH</i> for CRC risk and prognosis.</p><p><strong>Results: </strong>The expression levels of galectin-9 and <i>SHH</i> differed significantly between cancer tissues and adjacent normal tissues (<i>P</i><0.05). ROC analysis showed that the AUCs for galectin-9 and <i>SHH</i> in evaluating CRC risk were 0.809 (95% CI: 0.751-0.868) and 0.865 (95% CI: 0.817-0.912), respectively. Galectin-9 expression was lower in patients with T<sub>3-4</sub> stage, N<sub>1-3</sub> stage, M<sub>1</sub> stage, or poor differentiation (<i>P</i><0.05), whereas SHH expression was higher in these patients(<i>P</i><0.05). Galectin-9 expression was negatively correlated with <i>SHH</i> expression and TNM stage (<i>r</i>=－0.184 and －0.362, respectively; <i>P</i><0.001). <i>SHH</i> expression was positively correlated with TNM stage (<i>r</i> = 0.407, <i>P</i>< 0.001). Significant differences in galectin-9 and <i>SHH</i> expression were observed between patients with poor prognosis and those with good prognosis (<i>P</i>< 0.05). Logistic regression analysis indicated that T<sub>3-4</sub> stage (OR= 4.609, 95% CI: 1.461-14.535), poor differentiation (OR=3.337, 95% CI: 1.297-8.582), and high SHH expression (OR= 2.067, 95% CI: 1.162-3.678) were risk factors for poor prognosis (<i>P</i>< 0.05), while high galectin-9 expression (OR = 0.652, 95% CI: 0.437-0.975) was a protective factor (<i>P</i>< 0.05). The AUCs of galectin-9 and <i>SHH</i> for evaluating CRC prognosis were 0.769 (95% CI: 0.550-0.798) and 0.734 (95% CI: 0.603-0.866), respectively.</p><p><strong>Conclusion: </strong>Galectin-9 and SHH are lowly and highly expressed, respectively, in CRC. Their expression levels are associated with tumor differentiation, invasion, and metastasis, and hold predictive value for the risk and prognosis of CRC patients.</p>","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"217-223"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><strong>Objective: </strong>To systematically analyze the mutation spectrum of the androglobin gene (<i>ADGB</i>) in infertile males and investigate the association between its genotypes and phenotypes related to male infertility, thereby elucidating the critical role of ADGB in male reproductive function.</p><p><strong>Methods: </strong>This study recruited 781 Chinese males diagnosed with primary infertility. Whole exome sequencing (WES) combined with Sanger sequencing was used to screen for and identify potential pathogenic mutations in the <i>ADGB</i> gene among infertile males. Bioinformatics analysis of ADGB evolutionary conservation was conducted using MEGA11 software. Western blotting was performed to detect ADGB expression in patients' sperm. Semen analysis and modified Papanicolaou staining were used to evaluate sperm motility and morphological characteristics, while transmission electron microscopy (TEM) was used to observe abnormalities in sperm ultrastructure. Additionally, real-time fluorescence quantitative PCR was used to detect <i>Adgb</i> mRNA expression levels in various mouse tissues and testicular developmental stages. Immunofluorescence staining was used to analyze the localization and expression distribution of ADGB in human and mouse germ cells across different developmental stages. Finally, proteins associated with ADGB were screened using STRING data and validated by co-immunoprecipitation.</p><p><strong>Results: </strong>Among 781 infertile men, 148 <i>ADGB</i> gene mutation sites were identified. According to the American College of Medical Genetics and Genomics (ACMG) Variant Classification Guidelines, 45 sites were classified as benign mutations, one site as a potentially benign mutation, 96 sites as variants of uncertain significance, and 6 sites as potentially pathogenic mutations. Two potentially pathogenic mutations (c.4859G > A and c.4981A > G) were identified in a compound heterozygous state in a patient with idiopathic oligoasthenoteratozoospermia (OAT). Conservation analysis suggested that these mutations may disrupt functionally conserved domains of the <i>ADGB</i> gene across species, indicating potential pathogenicity. Western blot analysis revealed absent ADGB protein expression in the patient's sperm. Morphological analysis showed marked head abnormalities (microcephaly, conical heads) and tail defects (short tails, acutely angled curved tails, coiled tails, and tailless sperm) in the patient's sperm. TEM observations showed spermatozoa with acrosome loss, disorganized mitochondrial sheath helical structures, and disrupted or partially absent "9 + 2" microtubule structures in the axoneme. Additionally, ADGB was found to be highly expressed after puberty in both human and mouse testes and was localized to the acrosome and flagella of spermatogenic cells. Co-immunoprecipitation experiments confirmed TTC29 and CFAP47 as interacting proteins of ADGB. The patient carrying the pathogenic <i>ADGB</i> mutatio
{"title":"[Whole Exome Sequencing Identified Novel Pathogenic Mutations of <i>ADGB</i> in Patients With Oligoasthenozoospermia].","authors":"Qiuyi Wang, Yihong Yang, Chuan Jiang, Ying Shen","doi":"10.12182/20260160108","DOIUrl":"10.12182/20260160108","url":null,"abstract":"<p><strong>Objective: </strong>To systematically analyze the mutation spectrum of the androglobin gene (<i>ADGB</i>) in infertile males and investigate the association between its genotypes and phenotypes related to male infertility, thereby elucidating the critical role of ADGB in male reproductive function.</p><p><strong>Methods: </strong>This study recruited 781 Chinese males diagnosed with primary infertility. Whole exome sequencing (WES) combined with Sanger sequencing was used to screen for and identify potential pathogenic mutations in the <i>ADGB</i> gene among infertile males. Bioinformatics analysis of ADGB evolutionary conservation was conducted using MEGA11 software. Western blotting was performed to detect ADGB expression in patients' sperm. Semen analysis and modified Papanicolaou staining were used to evaluate sperm motility and morphological characteristics, while transmission electron microscopy (TEM) was used to observe abnormalities in sperm ultrastructure. Additionally, real-time fluorescence quantitative PCR was used to detect <i>Adgb</i> mRNA expression levels in various mouse tissues and testicular developmental stages. Immunofluorescence staining was used to analyze the localization and expression distribution of ADGB in human and mouse germ cells across different developmental stages. Finally, proteins associated with ADGB were screened using STRING data and validated by co-immunoprecipitation.</p><p><strong>Results: </strong>Among 781 infertile men, 148 <i>ADGB</i> gene mutation sites were identified. According to the American College of Medical Genetics and Genomics (ACMG) Variant Classification Guidelines, 45 sites were classified as benign mutations, one site as a potentially benign mutation, 96 sites as variants of uncertain significance, and 6 sites as potentially pathogenic mutations. Two potentially pathogenic mutations (c.4859G > A and c.4981A > G) were identified in a compound heterozygous state in a patient with idiopathic oligoasthenoteratozoospermia (OAT). Conservation analysis suggested that these mutations may disrupt functionally conserved domains of the <i>ADGB</i> gene across species, indicating potential pathogenicity. Western blot analysis revealed absent ADGB protein expression in the patient's sperm. Morphological analysis showed marked head abnormalities (microcephaly, conical heads) and tail defects (short tails, acutely angled curved tails, coiled tails, and tailless sperm) in the patient's sperm. TEM observations showed spermatozoa with acrosome loss, disorganized mitochondrial sheath helical structures, and disrupted or partially absent \"9 + 2\" microtubule structures in the axoneme. Additionally, ADGB was found to be highly expressed after puberty in both human and mouse testes and was localized to the acrosome and flagella of spermatogenic cells. Co-immunoprecipitation experiments confirmed TTC29 and CFAP47 as interacting proteins of ADGB. The patient carrying the pathogenic <i>ADGB</i> mutatio","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"160-169"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12979990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiaohua Xie, Derong Lin, Mei Li, Xiaolin Ye, Jingya Fang, Xiaowen Zhang, Aiguo Xue
Objective: To analyze trends in the disease burden of chronic respiratory diseases (CRD) attributable to smoking in China from 1990 to 2021 and to project its development from 2022 to 2035, providing scientific evidence for optimizing tobacco control strategies and public health decision-making.
Methods: Using Global Burden of Disease (GBD) 2021 data, epidemiological data on smoking-attributable CRD were collected for China, Japan, the European Union, the United States, and the global population from 1990 to 2021. Indicators included years lived with disability (YLDs), years of life lost (YLLs), and disability-adjusted life years (DALYs), covering individuals aged 30 years and older. Joinpoint regression models estimated average annual percentage changes (AAPCs), while Bayesian age-period-cohort (BAPC) models projected future trends.
Results: In 2021, smoking-attributable CRD DALYs in China reached 10320279 (95% uncertainty interval [UI]: 7806610-12875089) person-years, with an age-standardized disability-adjusted life years rate (ASDR) of 522.34 (95% UI: 394.50-653.32) per 100000 person-years. The number of deaths was 566446 (95% UI: 416802-720431), with an age-standardized mortality rate (ASMR) of 31.34 (95% UI: 23.10-39.69) per 100000 population. YLLs and YLDs were 8983486 (95% UI: 6547449-11421727) person-years and 1336793 (95% UI: 981768-1699656) person-years, corresponding to age-standardized rates (ASR) of 458.96 (95% UI: 337.53-582.19) per 100000 person-years and 63.38 (95% UI: 46.17-80.72) per 100000 person-years, respectively. The disease burden showed significant differences by gender and age, with higher risks among males and middle-aged and elderly populations. From 1990 to 2021, all burden indicators in China showed a declining trend, with ASMR and ASDR projected to continue decreasing over the next decade.
Conclusion: China has made positive progress in CRD prevention and tobacco control, but challenges such as population aging require continued attention. Targeted prevention interventions, particularly for high-risk populations, should be strengthened to reduce disease burden. The experience and challenges documented in China could offer valuable lessons and policy insights for other countries undergoing similar epidemiological transitions.
{"title":"[Analysis and Projection of the Burden of Chronic Respiratory Diseases Attributable to Smoking in China, 1990-2021].","authors":"Xiaohua Xie, Derong Lin, Mei Li, Xiaolin Ye, Jingya Fang, Xiaowen Zhang, Aiguo Xue","doi":"10.12182/20260160104","DOIUrl":"10.12182/20260160104","url":null,"abstract":"<p><strong>Objective: </strong>To analyze trends in the disease burden of chronic respiratory diseases (CRD) attributable to smoking in China from 1990 to 2021 and to project its development from 2022 to 2035, providing scientific evidence for optimizing tobacco control strategies and public health decision-making.</p><p><strong>Methods: </strong>Using Global Burden of Disease (GBD) 2021 data, epidemiological data on smoking-attributable CRD were collected for China, Japan, the European Union, the United States, and the global population from 1990 to 2021. Indicators included years lived with disability (YLDs), years of life lost (YLLs), and disability-adjusted life years (DALYs), covering individuals aged 30 years and older. Joinpoint regression models estimated average annual percentage changes (AAPCs), while Bayesian age-period-cohort (BAPC) models projected future trends.</p><p><strong>Results: </strong>In 2021, smoking-attributable CRD DALYs in China reached 10320279 (95% uncertainty interval [UI]: 7806610-12875089) person-years, with an age-standardized disability-adjusted life years rate (ASDR) of 522.34 (95% UI: 394.50-653.32) per 100000 person-years. The number of deaths was 566446 (95% UI: 416802-720431), with an age-standardized mortality rate (ASMR) of 31.34 (95% UI: 23.10-39.69) per 100000 population. YLLs and YLDs were 8983486 (95% UI: 6547449-11421727) person-years and 1336793 (95% UI: 981768-1699656) person-years, corresponding to age-standardized rates (ASR) of 458.96 (95% UI: 337.53-582.19) per 100000 person-years and 63.38 (95% UI: 46.17-80.72) per 100000 person-years, respectively. The disease burden showed significant differences by gender and age, with higher risks among males and middle-aged and elderly populations. From 1990 to 2021, all burden indicators in China showed a declining trend, with ASMR and ASDR projected to continue decreasing over the next decade.</p><p><strong>Conclusion: </strong>China has made positive progress in CRD prevention and tobacco control, but challenges such as population aging require continued attention. Targeted prevention interventions, particularly for high-risk populations, should be strengthened to reduce disease burden. The experience and challenges documented in China could offer valuable lessons and policy insights for other countries undergoing similar epidemiological transitions.</p>","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"209-216"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12979984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wangjieciren, Jun Lan, Dawazhuoma, Min Chen, Jinyang DU, Bengui Ye
<p><strong>Objective: </strong>The ameliorative effects of the ethanol extract of <i>Vicatia thibetica</i> de Boiss. (VTDB) on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced chronic atrophic gastritis (CAG) in rats were investigated, and its mechanism of action was preliminarily explored.</p><p><strong>Methods: </strong>Ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) was used to analyze the chemical constituents of VTDB. A rat CAG model was established using MNNG induction combined with irregular feeding. Seventy-two healthy male SD rats were randomly divided into six groups: normal control, model, low-dose VTDB (157 mg/[kg·d]), medium-dose VTDB (314 mg/[kg·d]), high-dose VTDB (628 mg/[kg·d]), and positive control (Vatacoenayme) (216 mg/[kg·d]), with 12 rats in each group. HE staining was used to observe pathological changes in the gastric mucosa of each group. ELISA was performed to measure serum levels of pepsinogen Ⅰ (PGⅠ), pepsinogen Ⅱ (PGⅡ), and inflammatory factors (TNF-α, IL-6, and IL-10). Levels of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in gastric tissues were determined. Western blot was used to measure the expression levels of heme oxygenase-1 (HO-1)/nuclear factor erythroid-2-related factor 2 (Nrf2) and myeloid differentiation primary response protein 88 (MyD88)/protein kinase B (AKT)/phosphatidylinositide 3-kinase (PI3K) signaling pathway proteins in gastric tissues.</p><p><strong>Results: </strong>By comparing retention times, mass spectral fragmentation patterns, and matching with the ESI (±)-MS/MS database, a total of 89 chemical constituents-primarily fatty acids, phenolic acids, and coumarins-were identified in VTDB. HE staining indicated that VTDB partially improved gastric mucosal damage in CAG rats. ELISA showed that, compared with the model group, the VTDB-treated groups had increased serum levels of PGⅠ, PGⅡ, and PGR (PGⅠ/PGⅡ) (<i>P</i> < 0.05) and decreased levels of gastrin 17 (G-17) (<i>P</i> < 0.05). In the low-, medium-, and high-dose groups, serum TNF-α levels decreased, and in the low- and high-dose groups, serum IL-6 secretion decreased (<i>P</i> < 0.05), while serum IL-10 secretion increased in the high-dose group (<i>P</i> < 0.001). In the VTDB medium- and high-dose groups, MDA levels in gastric tissue decreased (<i>P</i> < 0.01), and SOD activity increased in the VTDB low-, medium-, and high-dose groups (<i>P</i> < 0.05). Western blot results showed that HO-1 levels increased in the high-dose VTDB group and Nrf2 levels increased in the low-, medium-, and high-dose VTDB groups (<i>P</i> < 0.001). MyD88 levels decreased in the VTDB low- and high-dose groups, while AKT and PI3K levels decreased in the VTDB medium- and high-dose groups (<i>P</i> < 0.05), indicating that VTDB can modulate the expression of HO-1/Nrf2 and MyD88/AKT/PI3K signaling pathway proteins.</p><p><strong>Conclusion: </strong>VTDB reduces gastric damage and
{"title":"[Ethanol Extract of <i>Vicatia thibetica</i> de Boiss. Improves Chronic Atrophic Gastritis in Rats via the HO-1/Nrf2 and Myd88/AKT/PI3K Signaling Pathways].","authors":"Wangjieciren, Jun Lan, Dawazhuoma, Min Chen, Jinyang DU, Bengui Ye","doi":"10.12182/20260160107","DOIUrl":"10.12182/20260160107","url":null,"abstract":"<p><strong>Objective: </strong>The ameliorative effects of the ethanol extract of <i>Vicatia thibetica</i> de Boiss. (VTDB) on N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced chronic atrophic gastritis (CAG) in rats were investigated, and its mechanism of action was preliminarily explored.</p><p><strong>Methods: </strong>Ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) was used to analyze the chemical constituents of VTDB. A rat CAG model was established using MNNG induction combined with irregular feeding. Seventy-two healthy male SD rats were randomly divided into six groups: normal control, model, low-dose VTDB (157 mg/[kg·d]), medium-dose VTDB (314 mg/[kg·d]), high-dose VTDB (628 mg/[kg·d]), and positive control (Vatacoenayme) (216 mg/[kg·d]), with 12 rats in each group. HE staining was used to observe pathological changes in the gastric mucosa of each group. ELISA was performed to measure serum levels of pepsinogen Ⅰ (PGⅠ), pepsinogen Ⅱ (PGⅡ), and inflammatory factors (TNF-α, IL-6, and IL-10). Levels of malondialdehyde (MDA) and superoxide dismutase (SOD) activity in gastric tissues were determined. Western blot was used to measure the expression levels of heme oxygenase-1 (HO-1)/nuclear factor erythroid-2-related factor 2 (Nrf2) and myeloid differentiation primary response protein 88 (MyD88)/protein kinase B (AKT)/phosphatidylinositide 3-kinase (PI3K) signaling pathway proteins in gastric tissues.</p><p><strong>Results: </strong>By comparing retention times, mass spectral fragmentation patterns, and matching with the ESI (±)-MS/MS database, a total of 89 chemical constituents-primarily fatty acids, phenolic acids, and coumarins-were identified in VTDB. HE staining indicated that VTDB partially improved gastric mucosal damage in CAG rats. ELISA showed that, compared with the model group, the VTDB-treated groups had increased serum levels of PGⅠ, PGⅡ, and PGR (PGⅠ/PGⅡ) (<i>P</i> < 0.05) and decreased levels of gastrin 17 (G-17) (<i>P</i> < 0.05). In the low-, medium-, and high-dose groups, serum TNF-α levels decreased, and in the low- and high-dose groups, serum IL-6 secretion decreased (<i>P</i> < 0.05), while serum IL-10 secretion increased in the high-dose group (<i>P</i> < 0.001). In the VTDB medium- and high-dose groups, MDA levels in gastric tissue decreased (<i>P</i> < 0.01), and SOD activity increased in the VTDB low-, medium-, and high-dose groups (<i>P</i> < 0.05). Western blot results showed that HO-1 levels increased in the high-dose VTDB group and Nrf2 levels increased in the low-, medium-, and high-dose VTDB groups (<i>P</i> < 0.001). MyD88 levels decreased in the VTDB low- and high-dose groups, while AKT and PI3K levels decreased in the VTDB medium- and high-dose groups (<i>P</i> < 0.05), indicating that VTDB can modulate the expression of HO-1/Nrf2 and MyD88/AKT/PI3K signaling pathway proteins.</p><p><strong>Conclusion: </strong>VTDB reduces gastric damage and","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"97-106"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12979992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Respiratory syncytial virus (RSV) infection remains a leading cause of respiratory illness in infants and young children worldwide, with no widely available specific treatment. Advances in diagnostic technologies have increased the detection rate of RSV co-infections, but their impact on disease outcomes remains controversial. This work examines the epidemiological characteristics, clinical implications, and potential mechanisms of RSV co-infections. Findings indicate that RSV co-infections with bacteria or adenoviruses lead to more severe clinical symptoms and more complex treatment, while co-infections with other viruses may prolong illness without increasing severity. The specific mechanisms underlying RSV co-infections are still poorly understood. In recent years, significant breakthroughs in RSV vaccine and long-acting monoclonal antibody development have provided new tools for active prevention. Future research should focus on clarifying the molecular mechanisms of co-infections, developing targeted therapeutic drugs and vaccines, and optimizing diagnostic and treatment strategies to reduce the incidence and mortality of RSV-related diseases.
{"title":"[Epidemiology, Mechanisms, and Clinical Challenges of Respiratory Syncytial Virus Co-infections in Children].","authors":"Hongyuan Huang, Huilian Chen, Lina Qiao","doi":"10.12182/20260160506","DOIUrl":"10.12182/20260160506","url":null,"abstract":"<p><p>Respiratory syncytial virus (RSV) infection remains a leading cause of respiratory illness in infants and young children worldwide, with no widely available specific treatment. Advances in diagnostic technologies have increased the detection rate of RSV co-infections, but their impact on disease outcomes remains controversial. This work examines the epidemiological characteristics, clinical implications, and potential mechanisms of RSV co-infections. Findings indicate that RSV co-infections with bacteria or adenoviruses lead to more severe clinical symptoms and more complex treatment, while co-infections with other viruses may prolong illness without increasing severity. The specific mechanisms underlying RSV co-infections are still poorly understood. In recent years, significant breakthroughs in RSV vaccine and long-acting monoclonal antibody development have provided new tools for active prevention. Future research should focus on clarifying the molecular mechanisms of co-infections, developing targeted therapeutic drugs and vaccines, and optimizing diagnostic and treatment strategies to reduce the incidence and mortality of RSV-related diseases.</p>","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"277-284"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12979989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yingqing Lei, Hongbin Lü, Qi Zhou, Min Tian, Yang Cao
Objective: To quantitatively evaluate retinal microvascular changes in patients with diabetic retinopathy (DR) using optical coherence tomography angiography (OCTA), and to explore their association with blood-retinal barrier (BRB) disruption.
Methods: A total of 208 patients with type 2 diabetes and DR underwent OCTA to obtain microvascular parameters. Serum vascular endothelial growth factor (VEGF) and intercellular adhesion molecule 1 (ICAM-1) levels were measured. Correlations were analyzed, risk factors were identified using logistic regression, and diagnostic efficacy was evaluated with ROC curves.
Results: The superficial capillary density (SCP-D) and deep capillary density (DCP-D) of the 208 DR patients were (42.67 ± 4.35)% and (47.89 ± 5.02)%, respectively. The mean values for the area, perimeter, and circularity index of the foveal avascular zone (FAZ) were (0.38 ± 0.10) mm², (2.04 ± 0.28) mm, and 0.72 ± 0.08, respectively. The mean area of the non-perfusion zone was (1.87 ± 0.45) mm². Among these patients, 121 (58.17%) cases had abnormal SCP-D (< 45%), 114 (56.25%) cases had abnormal DCP-D (< 50%), 88 (42.31%) cases had abnormal FAZ area, 77 (37.02%) cases had abnormal FAZ perimeter, 69 (33.17%) cases had abnormal FAZ circularity index, and 142 (68.27%) cases had abnormal non-perfusion zone area. The FAZ area was positively correlated with VEGF (r = 0.559, 95% CI: 0.457-0.661) and ICAM-1 (r = 0.411, 95% CI: 0.289-0.533). The FAZ circularity index, SCP-D, and DCP-D were negatively correlated with VEGF and ICAM-1 (P < 0.05). The area of the non-perfusion zone was positively correlated with both. Logistic regression showed that the duration of diabetes (odds ratio [OR] = 1.159, 95% CI: 1.060-1.267) and VEGF (OR = 1.013, 95% CI: 1.005-1.022) were independent risk factors for severe retinal microvascular changes (P < 0.05). Among the four OCTA assessment indicators, the area of the non-perfusion zone had the highest predictive value, with an area under the curve (AUC) of 0.879 (95% CI: 0.820-0.938).
Conclusion: The OCTA assessment indicators in DR patients are closely related to BRB-related markers. The area of the non-perfusion zone has the highest predictive value for severe retinal microvascular changes in DR patients.
{"title":"[Quantitative Assessment of Microvascular Changes in Diabetic Retinopathy and Their Association With Blood-Retinal Barrier Impairment].","authors":"Yingqing Lei, Hongbin Lü, Qi Zhou, Min Tian, Yang Cao","doi":"10.12182/20260160504","DOIUrl":"10.12182/20260160504","url":null,"abstract":"<p><strong>Objective: </strong>To quantitatively evaluate retinal microvascular changes in patients with diabetic retinopathy (DR) using optical coherence tomography angiography (OCTA), and to explore their association with blood-retinal barrier (BRB) disruption.</p><p><strong>Methods: </strong>A total of 208 patients with type 2 diabetes and DR underwent OCTA to obtain microvascular parameters. Serum vascular endothelial growth factor (VEGF) and intercellular adhesion molecule 1 (ICAM-1) levels were measured. Correlations were analyzed, risk factors were identified using logistic regression, and diagnostic efficacy was evaluated with ROC curves.</p><p><strong>Results: </strong>The superficial capillary density (SCP-D) and deep capillary density (DCP-D) of the 208 DR patients were (42.67 ± 4.35)% and (47.89 ± 5.02)%, respectively. The mean values for the area, perimeter, and circularity index of the foveal avascular zone (FAZ) were (0.38 ± 0.10) mm², (2.04 ± 0.28) mm, and 0.72 ± 0.08, respectively. The mean area of the non-perfusion zone was (1.87 ± 0.45) mm². Among these patients, 121 (58.17%) cases had abnormal SCP-D (< 45%), 114 (56.25%) cases had abnormal DCP-D (< 50%), 88 (42.31%) cases had abnormal FAZ area, 77 (37.02%) cases had abnormal FAZ perimeter, 69 (33.17%) cases had abnormal FAZ circularity index, and 142 (68.27%) cases had abnormal non-perfusion zone area. The FAZ area was positively correlated with VEGF (<i>r</i> = 0.559, 95% CI: 0.457-0.661) and ICAM-1 (<i>r</i> = 0.411, 95% CI: 0.289-0.533). The FAZ circularity index, SCP-D, and DCP-D were negatively correlated with VEGF and ICAM-1 (<i>P</i> < 0.05). The area of the non-perfusion zone was positively correlated with both. Logistic regression showed that the duration of diabetes (odds ratio [OR] = 1.159, 95% CI: 1.060-1.267) and VEGF (OR = 1.013, 95% CI: 1.005-1.022) were independent risk factors for severe retinal microvascular changes (<i>P</i> < 0.05). Among the four OCTA assessment indicators, the area of the non-perfusion zone had the highest predictive value, with an area under the curve (AUC) of 0.879 (95% CI: 0.820-0.938).</p><p><strong>Conclusion: </strong>The OCTA assessment indicators in DR patients are closely related to BRB-related markers. The area of the non-perfusion zone has the highest predictive value for severe retinal microvascular changes in DR patients.</p>","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"154-159"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980006/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective: To investigate whether the novel proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor Inclisiran exerts protective effects on the kidneys under high-glucose conditions, and to predict whether its mechanism involves the transforming growth factor-β (TGF-β) pathway using proteomic techniques, while constructing its regulatory network.
Methods: Healthy male C57BL/6J mice were randomly assigned to four groups: Group A (control, n = 9), Group B (diabetes model, n = 9), Group C (diabetes + low-dose Inclisiran, n = 9), and Group D (diabetes + high-dose Inclisiran, n = 9). Groups B, C, and D were induced with type 2 diabetes using a high-fat diet combined with streptozotocin (STZ). Diabetes was confirmed by three consecutive days of fasting blood glucose levels > 16.7 mmol/L after modeling. The experiment ended 8 weeks after modeling. Renal tissue changes were evaluated using hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining. Serum creatinine, low-density lipoprotein (LDL), cholesterol, and PCSK9 levels were measured, along with 24 h urinary protein-to-creatinine ratios. Renal tissue samples from Groups A, B, and D (4 mice per group) underwent transcriptomic sequencing to identify differentially expressed proteins. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to assess the potential of Inclisiran to protect the kidneys via the TGF-β pathway.
Results: After modeling, blood glucose, urine protein/creatinine ratio, blood creatinine, cholesterol, and other indicators in groups B, C, and D were significantly higher than those in group A, with group B showing the highest values (P < 0.05). In the renal tissues of groups B, C, and D, focal tubular cell degeneration and mesangial proliferation were observed. The glomerular proliferation index in group B was significantly higher than in the other groups. Proteomics identified 1096 differentially expressed proteins (579 upregulated and 517 downregulated) between groups A and B, and 911 differentially expressed proteins (475 upregulated and 436 downregulated) between groups B and D. KEGG enrichment analysis showed that the TGF-β pathway was enriched in both the A-B and B-D group comparisons. There were 11 downregulated differentially expressed proteins (P45481: Crebbp, P70387: Hfe, Q61502: E2f5, Q62312: Tgfbr2, Q62432: Smad2, Q8BSK8: Rps6kb1, Q8BUN5: Smad3, Q8CG19: Ltbp1, Q9CUN6: Smurf1, Q9JKX3: Tfr2, Q9Z1M4: Rps6kb2) related to this pathway between groups B and D.
Conclusion: Inclisiran may improve the lipid profile of type 2 diabetic mice and reduce the activity of the TGF-β pathway. Its mechanism of action may be related to effects such as extracellular matrix proliferation.
{"title":"[Study of the Protective Effect and Mechanism of Inclisiran on Renal Tissue in a Type 2 Diabetes Mouse Model via the Transforming Growth Factor-β Pathway].","authors":"Hongqian Li, Bo Chen, Xin Xiang, Ling Qi, Dongmei Zhang, Yuhan Tang, Liling Zhang, Santao Ou, Ling Xue, Weihua Wu","doi":"10.12182/20260160507","DOIUrl":"10.12182/20260160507","url":null,"abstract":"<p><strong>Objective: </strong>To investigate whether the novel proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor Inclisiran exerts protective effects on the kidneys under high-glucose conditions, and to predict whether its mechanism involves the transforming growth factor-β (TGF-β) pathway using proteomic techniques, while constructing its regulatory network.</p><p><strong>Methods: </strong>Healthy male C57BL/6J mice were randomly assigned to four groups: Group A (control, <i>n</i> = 9), Group B (diabetes model, <i>n</i> = 9), Group C (diabetes + low-dose Inclisiran, <i>n</i> = 9), and Group D (diabetes + high-dose Inclisiran, <i>n</i> = 9). Groups B, C, and D were induced with type 2 diabetes using a high-fat diet combined with streptozotocin (STZ). Diabetes was confirmed by three consecutive days of fasting blood glucose levels > 16.7 mmol/L after modeling. The experiment ended 8 weeks after modeling. Renal tissue changes were evaluated using hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining. Serum creatinine, low-density lipoprotein (LDL), cholesterol, and PCSK9 levels were measured, along with 24 h urinary protein-to-creatinine ratios. Renal tissue samples from Groups A, B, and D (4 mice per group) underwent transcriptomic sequencing to identify differentially expressed proteins. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were performed to assess the potential of Inclisiran to protect the kidneys via the TGF-β pathway.</p><p><strong>Results: </strong>After modeling, blood glucose, urine protein/creatinine ratio, blood creatinine, cholesterol, and other indicators in groups B, C, and D were significantly higher than those in group A, with group B showing the highest values (<i>P</i> < 0.05). In the renal tissues of groups B, C, and D, focal tubular cell degeneration and mesangial proliferation were observed. The glomerular proliferation index in group B was significantly higher than in the other groups. Proteomics identified 1096 differentially expressed proteins (579 upregulated and 517 downregulated) between groups A and B, and 911 differentially expressed proteins (475 upregulated and 436 downregulated) between groups B and D. KEGG enrichment analysis showed that the TGF-β pathway was enriched in both the A-B and B-D group comparisons. There were 11 downregulated differentially expressed proteins (P45481: Crebbp, P70387: Hfe, Q61502: E2f5, Q62312: Tgfbr2, Q62432: Smad2, Q8BSK8: Rps6kb1, Q8BUN5: Smad3, Q8CG19: Ltbp1, Q9CUN6: Smurf1, Q9JKX3: Tfr2, Q9Z1M4: Rps6kb2) related to this pathway between groups B and D.</p><p><strong>Conclusion: </strong>Inclisiran may improve the lipid profile of type 2 diabetic mice and reduce the activity of the TGF-β pathway. Its mechanism of action may be related to effects such as extracellular matrix proliferation.</p>","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"132-138"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12979993/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zucen Li, Chunyi Xu, Ruoshi Xu, Chenchen Zhou, Yi Fan
Adipose tissue, a vital component of the human body, serves multiple functions, including energy storage, thermal insulation, and protection. Fat is a highly active, dynamic organ that communicates with other organs, playing a crucial role in maintaining health and is closely linked to the onset and progression of diseases. Chronic diseases associated with adipose tissue result from dysregulated inter-organ interactions and have become a major public health challenge. A systematic review of regulatory networks centered on adipose tissue could help overcome the limitations of single-organ studies and identify key inter-organ communication pathways. This article reviews recent advances regarding adipose tissue as a pivotal signaling hub that facilitates inter-organ communication with the liver, gut, brain, and bone, as well as its connection to tumor progression. The review also highlights the applications of cutting-edge technologies such as single-cell sequencing and artificial intelligence in adipose tissue research. Continued exploration of the crosstalk between adipose tissue and other organs holds great potential for disease treatment and health management.
{"title":"[Recent Advances in the Interorgan Regulatory Roles of Adipose Tissue].","authors":"Zucen Li, Chunyi Xu, Ruoshi Xu, Chenchen Zhou, Yi Fan","doi":"10.12182/20260160201","DOIUrl":"10.12182/20260160201","url":null,"abstract":"<p><p>Adipose tissue, a vital component of the human body, serves multiple functions, including energy storage, thermal insulation, and protection. Fat is a highly active, dynamic organ that communicates with other organs, playing a crucial role in maintaining health and is closely linked to the onset and progression of diseases. Chronic diseases associated with adipose tissue result from dysregulated inter-organ interactions and have become a major public health challenge. A systematic review of regulatory networks centered on adipose tissue could help overcome the limitations of single-organ studies and identify key inter-organ communication pathways. This article reviews recent advances regarding adipose tissue as a pivotal signaling hub that facilitates inter-organ communication with the liver, gut, brain, and bone, as well as its connection to tumor progression. The review also highlights the applications of cutting-edge technologies such as single-cell sequencing and artificial intelligence in adipose tissue research. Continued exploration of the crosstalk between adipose tissue and other organs holds great potential for disease treatment and health management.</p>","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"291-298"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12979987/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The microecological theory represents the current understanding of dental caries etiology, emphasizing that the dynamic balance of the structure and function of the oral microbial community plays a central role in the initiation and progression of caries. This theory posits that dental caries is not caused by a single specific pathogen, but rather results from dysbiosis-an imbalance-of the entire oral microecosystem. By redefining caries from an "infectious disease" to an "ecological imbalance disorder," the microecological theory offers a novel perspective for caries prevention, early intervention, and precision treatment. It underscores that maintaining the homeostasis of the oral microecology is more critical than simply eradicating bacteria, and that ecological approaches represent a key strategy for population-level caries prevention. Homeostatic medicine emphasizes that the dynamic equilibrium of the body's internal environment is fundamental to health. As a major microbial habitat and immunological interface, the oral cavity plays a pivotal role in the body's overall homeostatic network. The stability of the oral microbiome is thus a crucial node in systemic homeostasis. Homeostatic medicine provides a systems-oriented framework for understanding dental caries, shifting the paradigm ofcaries management from "fighting pathogens "toward "preserving ecological balance". This integrative approach aims to achieve the broader goal of promoting systemic homeostasis through local oral health promotion.
{"title":"[The Oral Microecological Theory of Dental Caries].","authors":"Xuedong Zhou","doi":"10.12182/20260160301","DOIUrl":"10.12182/20260160301","url":null,"abstract":"<p><p>The microecological theory represents the current understanding of dental caries etiology, emphasizing that the dynamic balance of the structure and function of the oral microbial community plays a central role in the initiation and progression of caries. This theory posits that dental caries is not caused by a single specific pathogen, but rather results from dysbiosis-an imbalance-of the entire oral microecosystem. By redefining caries from an \"infectious disease\" to an \"ecological imbalance disorder,\" the microecological theory offers a novel perspective for caries prevention, early intervention, and precision treatment. It underscores that maintaining the homeostasis of the oral microecology is more critical than simply eradicating bacteria, and that ecological approaches represent a key strategy for population-level caries prevention. Homeostatic medicine emphasizes that the dynamic equilibrium of the body's internal environment is fundamental to health. As a major microbial habitat and immunological interface, the oral cavity plays a pivotal role in the body's overall homeostatic network. The stability of the oral microbiome is thus a crucial node in systemic homeostasis. Homeostatic medicine provides a systems-oriented framework for understanding dental caries, shifting the paradigm ofcaries management from \"fighting pathogens \"toward \"preserving ecological balance\". This integrative approach aims to achieve the broader goal of promoting systemic homeostasis through local oral health promotion.</p>","PeriodicalId":39321,"journal":{"name":"四川大学学报(医学版)","volume":"57 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147463995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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