Direct current (DC) is a direction-constant current, and the research on its biological mechanism is expanding from traditional physical therapy to the field of precision medicine. This comprehensive review systematically summarizes the physical properties of DC and its core biological effects (ion migration, electroosmosis, and electrophoresis) and focuses on the cellular mechanisms and clinical applications in tissue repair and regeneration (e.g., wound healing and angiogenesis) and neurological disease treatment (e.g., modulation of neuroplasticity by transcranial DC stimulation). This review focuses on the field of ophthalmology, where DC stimulation has been shown to promote orderly corneal repair, modulate aqueous humor dynamics to reduce intraocular pressure in patients with glaucoma, and ameliorate retinal degenerative diseases and central visual dysfunction. Although DC therapy in ophthalmology has shown unique advantages, including precise targeting, minimal invasiveness, synergistic drug enhancement, and regenerative potential, its clinical translation still faces challenges in safety control, precise targeted delivery, and individualized treatment. In the future, it is necessary to promote the integration of medical and engineering fields, explore electro-drug synergistic strategies, develop intelligent closed-loop systems, and standardize clinical protocols, so as to provide new solutions to break through the bottleneck of the treatment of refractory ocular disease.
{"title":"Research and application of direct current in medicine: From cellular and molecular mechanisms to clinical application in ophthalmology.","authors":"Chunyang Cai, Yuntian Wan, Qingquan Wei, Xinyi Lai, Qinghua Qiu","doi":"10.1016/j.biocel.2026.106908","DOIUrl":"10.1016/j.biocel.2026.106908","url":null,"abstract":"<p><p>Direct current (DC) is a direction-constant current, and the research on its biological mechanism is expanding from traditional physical therapy to the field of precision medicine. This comprehensive review systematically summarizes the physical properties of DC and its core biological effects (ion migration, electroosmosis, and electrophoresis) and focuses on the cellular mechanisms and clinical applications in tissue repair and regeneration (e.g., wound healing and angiogenesis) and neurological disease treatment (e.g., modulation of neuroplasticity by transcranial DC stimulation). This review focuses on the field of ophthalmology, where DC stimulation has been shown to promote orderly corneal repair, modulate aqueous humor dynamics to reduce intraocular pressure in patients with glaucoma, and ameliorate retinal degenerative diseases and central visual dysfunction. Although DC therapy in ophthalmology has shown unique advantages, including precise targeting, minimal invasiveness, synergistic drug enhancement, and regenerative potential, its clinical translation still faces challenges in safety control, precise targeted delivery, and individualized treatment. In the future, it is necessary to promote the integration of medical and engineering fields, explore electro-drug synergistic strategies, develop intelligent closed-loop systems, and standardize clinical protocols, so as to provide new solutions to break through the bottleneck of the treatment of refractory ocular disease.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"106908"},"PeriodicalIF":2.8,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146097146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-23DOI: 10.1016/j.biocel.2026.106907
Yanhong Guo , Silu Zhao , Xuewen Zhang, Liuwei Wang, Yulin Wang, Qiuhong Li, Zihan Zhai, Lu Yu, Lin Tang
Background
Peritoneal fibrosis is a serious complication of long-term peritoneal dialysis (PD). Previous studies have demonstrated that circular RNAs (circRNAs) play an important role in organ fibrosis. However, whether circRNAs are involved in the progression of peritoneal fibrosis remains largely elusive. This study aimed to investigate the role of circRNAs in peritoneal fibrosis and clarify the underlying mechanisms.
Methods
CircRNA expression in peritoneal mesothelial cells derived from peritoneal dialysis effluent was profiled using a human circRNA microarray. The function of circTHBS1 was studied through gene silencing and overexpression. qRT-PCR and western blotting were used to detect the expression of relevant molecules. PD mouse models with adeno-associated virus (AAV)-mediated circTHBS1 knockdown were established to investigate the role of circTHBS1 in peritoneal fibrosis using histological staining and peritoneal function analyses.
Results
CircTHBS1 was significantly upregulated in peritoneal mesothelial cells from long-term PD patients and was positively correlated with the expression of fibronectin, alpha-smooth muscle actin (α-SMA), and connective tissue growth factor (CTGF). Silencing circTHBS1 suppressed epithelial-mesenchymal transition (EMT) in HMrSV5 cells. In vivo, circTHBS1 knockdown significantly alleviated peritoneal thickening and fibrosis, lowered α-SMA expression, and improved peritoneal function in PD mice. Mechanistically, circTHBS1 acted as a sponge for miR-18a-5p, relieving its repression of CTGF, and directly interacted with CTGF, thereby enhancing its stability. CTGF silencing partially attenuated EMT induced by circTHBS1 overexpression and miR-18a-5p inhibition.
Conclusion
This study suggests that circTHBS1 could be a candidate target for the treatment of peritoneal fibrosis.
{"title":"CircTHBS1 aggravates peritoneal fibrosis by sponging miR-18a-5p and interacting with CTGF","authors":"Yanhong Guo , Silu Zhao , Xuewen Zhang, Liuwei Wang, Yulin Wang, Qiuhong Li, Zihan Zhai, Lu Yu, Lin Tang","doi":"10.1016/j.biocel.2026.106907","DOIUrl":"10.1016/j.biocel.2026.106907","url":null,"abstract":"<div><h3>Background</h3><div>Peritoneal fibrosis is a serious complication of long-term peritoneal dialysis (PD). Previous studies have demonstrated that circular RNAs (circRNAs) play an important role in organ fibrosis. However, whether circRNAs are involved in the progression of peritoneal fibrosis remains largely elusive. This study aimed to investigate the role of circRNAs in peritoneal fibrosis and clarify the underlying mechanisms.</div></div><div><h3>Methods</h3><div>CircRNA expression in peritoneal mesothelial cells derived from peritoneal dialysis effluent was profiled using a human circRNA microarray. The function of circTHBS1 was studied through gene silencing and overexpression. qRT-PCR and western blotting were used to detect the expression of relevant molecules. PD mouse models with adeno-associated virus (AAV)-mediated circTHBS1 knockdown were established to investigate the role of circTHBS1 in peritoneal fibrosis using histological staining and peritoneal function analyses.</div></div><div><h3>Results</h3><div>CircTHBS1 was significantly upregulated in peritoneal mesothelial cells from long-term PD patients and was positively correlated with the expression of fibronectin, alpha-smooth muscle actin (α-SMA), and connective tissue growth factor (CTGF). Silencing circTHBS1 suppressed epithelial-mesenchymal transition (EMT) in HMrSV5 cells. In vivo, circTHBS1 knockdown significantly alleviated peritoneal thickening and fibrosis, lowered α-SMA expression, and improved peritoneal function in PD mice. Mechanistically, circTHBS1 acted as a sponge for miR-18a-5p, relieving its repression of CTGF, and directly interacted with CTGF, thereby enhancing its stability. CTGF silencing partially attenuated EMT induced by circTHBS1 overexpression and miR-18a-5p inhibition.</div></div><div><h3>Conclusion</h3><div>This study suggests that circTHBS1 could be a candidate target for the treatment of peritoneal fibrosis.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"193 ","pages":"Article 106907"},"PeriodicalIF":2.8,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146045204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-23DOI: 10.1016/j.biocel.2026.106906
Shixian Zhai, Zihong Huang, Chunchun An, Lu Gao, Tongsheng Chen
Mitofusin 2 (MFN2) has been reported to play an important role in mitophagy, but how MFN2 mediates mitophagy remains incompletely understood. Here, we establish that MFN2 upregulation is a key driver of mitophagy in MCF-7 cells. MFN2 overexpression triggers mitochondrial degradation, as verified by multiple mitophagy markers, whereas MFN2 knockdown abolishes the mitophagic response induced by Leflunomide (Lef), a compound that promotes mitophagy by upregulating MFN2. To elucidate the underlying mechanism, fluorescence imaging and subcellular fractionation reveal that MFN2 promotes AMP-activated protein kinase (AMPK) phosphorylation at Thr172 and facilitates translocation of AMPK from the cytoplasm to mitochondria. Quantitative Förster resonance energy transfer (FRET) analysis supports phosphorylation-dependent formation of an MFN2-AMPK complex in cells, and site-directed mutagenesis supports Thr172 phosphorylation dependence, as the phosphomimetic AMPK (T172D) mutant exhibits enhanced complex formation with MFN2, while the phosphodeficient AMPK (T172A) mutant shows little or no complex formation with MFN2. Co-immunoprecipitation further supports an MFN2-AMPK complex in cells. The MFN2-AMPK complex is essential for mitophagy: Compound C, a pharmacological inhibitor of AMPK, prevents both MFN2-AMPK complex formation and mitophagy, even in cells overexpressing MFN2. Notably, AMPK activation through Acadesine (AICAR) treatment is insufficient to induce mitophagy, but it markedly enhances mitophagy markers when combined with MFN2 overexpression. In conclusion, MFN2 mediates efficient mitophagy by recruiting Thr172-phosphorylated AMPK to mitochondria through a phosphorylation-dependent MFN2-AMPK complex.
{"title":"MFN2 interacts with phosphorylated AMPK to mediate mitophagy in MCF-7 cells.","authors":"Shixian Zhai, Zihong Huang, Chunchun An, Lu Gao, Tongsheng Chen","doi":"10.1016/j.biocel.2026.106906","DOIUrl":"10.1016/j.biocel.2026.106906","url":null,"abstract":"<p><p>Mitofusin 2 (MFN2) has been reported to play an important role in mitophagy, but how MFN2 mediates mitophagy remains incompletely understood. Here, we establish that MFN2 upregulation is a key driver of mitophagy in MCF-7 cells. MFN2 overexpression triggers mitochondrial degradation, as verified by multiple mitophagy markers, whereas MFN2 knockdown abolishes the mitophagic response induced by Leflunomide (Lef), a compound that promotes mitophagy by upregulating MFN2. To elucidate the underlying mechanism, fluorescence imaging and subcellular fractionation reveal that MFN2 promotes AMP-activated protein kinase (AMPK) phosphorylation at Thr172 and facilitates translocation of AMPK from the cytoplasm to mitochondria. Quantitative Förster resonance energy transfer (FRET) analysis supports phosphorylation-dependent formation of an MFN2-AMPK complex in cells, and site-directed mutagenesis supports Thr172 phosphorylation dependence, as the phosphomimetic AMPK (T172D) mutant exhibits enhanced complex formation with MFN2, while the phosphodeficient AMPK (T172A) mutant shows little or no complex formation with MFN2. Co-immunoprecipitation further supports an MFN2-AMPK complex in cells. The MFN2-AMPK complex is essential for mitophagy: Compound C, a pharmacological inhibitor of AMPK, prevents both MFN2-AMPK complex formation and mitophagy, even in cells overexpressing MFN2. Notably, AMPK activation through Acadesine (AICAR) treatment is insufficient to induce mitophagy, but it markedly enhances mitophagy markers when combined with MFN2 overexpression. In conclusion, MFN2 mediates efficient mitophagy by recruiting Thr172-phosphorylated AMPK to mitochondria through a phosphorylation-dependent MFN2-AMPK complex.</p>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":" ","pages":"106906"},"PeriodicalIF":2.8,"publicationDate":"2026-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146047318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-28DOI: 10.1016/j.biocel.2025.106896
María Alejandra Sánchez-Muñoz , Adriana Castillo-Villanueva , Marcia Rosario Pérez-Dosal , Bertha Molina-Álvarez , Salvador Uribe-Carvajal , Diego González-Halphen , Isabel Medina-Vera , Horacio Reyes-Vivas , Jesús Oria-Hernández
Mitochondriopathies often lead to chronic degenerative pathology. Muscle biopsy is considered the gold standard for diagnosis; however, its invasiveness restricts the amount of tissue obtained, and issue that is limiting for prospective, longitudinal, and pharmacological studies. Primary human fibroblasts (HF) lines are a valid alternative to biochemically characterize mitochondrial syndromes. Cell disruption is essential for measuring mitochondrial enzyme activity, and yet, no systematic comparative study has evaluated the different existing methods. Using 17 different cell lysis procedures, we evaluated the activity preservation of two mitochondrial enzymes: complex IV or cytochrome c oxidase (CIV) and citrate synthase (CS), in normal HF samples from pediatric patients. Procedures were categorized as chemical, mechanical, physical, and enzymatic. Only the enzymatic disruption using Pronase leads to high activity values for both CIV and CS activities, exhibiting intra- and inter-sample consistency. We then measured the activities of all mitochondrial complexes (CI, CI+CIII, CII, CII+CIII) and CV (ATP hydrolysis) in Pronase-disrupted cells, finding proper reproducibility and values comparable to those in the literature. We propose Pronase cell disruption is an adequate method for evaluating mitochondrial activities in HF samples.
{"title":"Comparison of disruption methods to optimize the evaluation of mitochondrial enzymatic activities in human fibroblasts","authors":"María Alejandra Sánchez-Muñoz , Adriana Castillo-Villanueva , Marcia Rosario Pérez-Dosal , Bertha Molina-Álvarez , Salvador Uribe-Carvajal , Diego González-Halphen , Isabel Medina-Vera , Horacio Reyes-Vivas , Jesús Oria-Hernández","doi":"10.1016/j.biocel.2025.106896","DOIUrl":"10.1016/j.biocel.2025.106896","url":null,"abstract":"<div><div>Mitochondriopathies often lead to chronic degenerative pathology. Muscle biopsy is considered the gold standard for diagnosis; however, its invasiveness restricts the amount of tissue obtained, and issue that is limiting for prospective, longitudinal, and pharmacological studies. Primary human fibroblasts (HF) lines are a valid alternative to biochemically characterize mitochondrial syndromes. Cell disruption is essential for measuring mitochondrial enzyme activity, and yet, no systematic comparative study has evaluated the different existing methods. Using 17 different cell lysis procedures, we evaluated the activity preservation of two mitochondrial enzymes: complex IV or cytochrome <em>c</em> oxidase (CIV) and citrate synthase (CS), in normal HF samples from pediatric patients. Procedures were categorized as chemical, mechanical, physical, and enzymatic. Only the enzymatic disruption using Pronase leads to high activity values for both CIV and CS activities, exhibiting intra- and inter-sample consistency. We then measured the activities of all mitochondrial complexes (CI, CI+CIII, CII, CII+CIII) and CV (ATP hydrolysis) in Pronase-disrupted cells, finding proper reproducibility and values comparable to those in the literature. We propose Pronase cell disruption is an adequate method for evaluating mitochondrial activities in HF samples.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"191 ","pages":"Article 106896"},"PeriodicalIF":2.8,"publicationDate":"2025-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145866194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-19DOI: 10.1016/j.biocel.2025.106895
Qing-Xin Wei , Nasar Khan , Xi-Jun Yin
This study investigated the therapeutic potential of exosomes derived from fetal muscle stem cells (FMSC-Exos) in mitigating dexamethasone (DEX)-induced muscle atrophy in a mouse model. Kunming (KM) mice were utilized to visualize muscle atrophy at the single muscle fiber level through an optimized isolation technique. Following the induction of muscle atrophy by dexamethasone, mice were treated with FMSC-Exos via local intramuscular injection into the gastrocnemius muscle. Results demonstrated that exosome administration showed a trend towards improved body weight and significantly increased muscle mass and individual muscle fiber diameter compared to the dexamethasone-only group. Histological analysis confirmed that FMSC-Exos effectively alleviated muscle fiber atrophy and promoted regeneration. RT-PCR and Western blot analyses revealed differential expression of the muscle atrophy markers MuRF1 and MAFbx/Atrogin-1. The mRNA expression levels of these atrophy-related factors were significantly elevated in the DEX-treated group compared to the control. Although expression levels in the exosome treatment group remained higher than control, they were significantly lower than in the DEX group. Protein expression followed a similar trend, indicating that dexamethasone modulates MuRF1 and MAFbx at both transcriptional and translational levels, and that exosome treatment counteracts this effect, promoting a restoration towards normal muscle protein expression homeostasis.
{"title":"Fetal muscle stem cell-derived exosomes improve dexamethasone-induced muscle atrophy at the single muscle fiber level","authors":"Qing-Xin Wei , Nasar Khan , Xi-Jun Yin","doi":"10.1016/j.biocel.2025.106895","DOIUrl":"10.1016/j.biocel.2025.106895","url":null,"abstract":"<div><div>This study investigated the therapeutic potential of exosomes derived from fetal muscle stem cells (FMSC-Exos) in mitigating dexamethasone (DEX)-induced muscle atrophy in a mouse model. Kunming (KM) mice were utilized to visualize muscle atrophy at the single muscle fiber level through an optimized isolation technique. Following the induction of muscle atrophy by dexamethasone, mice were treated with FMSC-Exos via local intramuscular injection into the gastrocnemius muscle. Results demonstrated that exosome administration showed a trend towards improved body weight and significantly increased muscle ma<strong>ss</strong> and individual muscle fiber diameter compared to the dexamethasone-only group. Histological analysis confirmed that FMSC-Exos effectively alleviated muscle fiber atrophy and promoted regeneration. RT-PCR and Western blot analyses revealed differential expression of the muscle atrophy markers MuRF1 and MAFbx/Atrogin-1. The mRNA expression levels of these atrophy-related factors were significantly elevated in the DEX-treated group compared to the control. Although expression levels in the exosome treatment group remained higher than control, they were significantly lower than in the DEX group. Protein expression followed a similar trend, indicating that dexamethasone modulates MuRF1 and MAFbx at both transcriptional and translational levels, and that exosome treatment counteracts this effect, promoting a restoration towards normal muscle protein expression homeostasis.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"191 ","pages":"Article 106895"},"PeriodicalIF":2.8,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145806337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-04DOI: 10.1016/j.biocel.2025.106894
Yang Li , Jingjing Zhao , Mubai Li , Yinglong Cheng , Li Liu
Background
Persistent high-risk human papilloma virus (HR-HPV) infection is a key factor in the progression of cervical lesions to cervical cancer. This study explores the molecular mechanisms through which the traditional Chinese medicine Xiaoyou Decoction (XYD) inhibits cervical intraepithelial neoplasia (CIN) lesions, offering new insights into its potential therapeutic application.
Materials and methods
Network pharmacology analysis was employed to identify the potential active ingredients and key target genes of XYD in treating CIN. Functional enrichment analysis was utilized to pinpoint the critical biological pathways affected by XYD. Clinical randomized trials were performed to evaluate the clinical efficacy of XYD. In vitro experiments were conducted to explore the functional effects and underlying molecular mechanisms of XYD.
Results
A total of 209 potential target genes of XYD associated with CIN lesions were identified. In addition, the active ingredients of XYD exhibited a strong association with autophagy-related proteins. Clinical randomized trials demonstrated that XYD treatment effectively alleviated HR-HPV infection, and after a 6-month follow-up, 90.3 % of patients exhibited negative conversion, successfully reversing the progression of CIN lesions. In vitro experiments confirmed that XYD inhibited CIN cell proliferation by activating the autophagy pathway and upregulating p53 protein expression.
Conclusion
In conclusion, our study reveals that XYD effectively prevents the persistence of HR-HPV infection and reverses the progression of CIN lesions by activating the autophagy pathway and upregulating p53 expression. These findings provide preliminary insights into the biological effects and specific mechanisms of XYD in CIN, offering a novel perspective for treating persistent HR-HPV infections.
{"title":"Xiaoyou decoction suppresses cervical precancerous lesions through the activation of cellular autophagy and the upregulation of p53 expression","authors":"Yang Li , Jingjing Zhao , Mubai Li , Yinglong Cheng , Li Liu","doi":"10.1016/j.biocel.2025.106894","DOIUrl":"10.1016/j.biocel.2025.106894","url":null,"abstract":"<div><h3>Background</h3><div>Persistent high-risk human papilloma virus (HR-HPV) infection is a key factor in the progression of cervical lesions to cervical cancer. This study explores the molecular mechanisms through which the traditional Chinese medicine Xiaoyou Decoction (XYD) inhibits cervical intraepithelial neoplasia (CIN) lesions, offering new insights into its potential therapeutic application.</div></div><div><h3>Materials and methods</h3><div>Network pharmacology analysis was employed to identify the potential active ingredients and key target genes of XYD in treating CIN. Functional enrichment analysis was utilized to pinpoint the critical biological pathways affected by XYD. Clinical randomized trials were performed to evaluate the clinical efficacy of XYD. In vitro experiments were conducted to explore the functional effects and underlying molecular mechanisms of XYD.</div></div><div><h3>Results</h3><div>A total of 209 potential target genes of XYD associated with CIN lesions were identified. In addition, the active ingredients of XYD exhibited a strong association with autophagy-related proteins. Clinical randomized trials demonstrated that XYD treatment effectively alleviated HR-HPV infection, and after a 6-month follow-up, 90.3 % of patients exhibited negative conversion, successfully reversing the progression of CIN lesions. In vitro experiments confirmed that XYD inhibited CIN cell proliferation by activating the autophagy pathway and upregulating p53 protein expression.</div></div><div><h3>Conclusion</h3><div>In conclusion, our study reveals that XYD effectively prevents the persistence of HR-HPV infection and reverses the progression of CIN lesions by activating the autophagy pathway and upregulating p53 expression. These findings provide preliminary insights into the biological effects and specific mechanisms of XYD in CIN, offering a novel perspective for treating persistent HR-HPV infections.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"191 ","pages":"Article 106894"},"PeriodicalIF":2.8,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-12-01DOI: 10.1016/j.biocel.2025.106877
Meiqi Sun , Hua Fang , Jiashu Zhang , Mengyao Wang , Peng Jiang , LiLi Ma , Huanyu Jin , Wei Zhang
{"title":"Corrigendum to “Resistance to silicosis progression in mice with Ch25h downregulation: The involvement of NLRP3 inflammasome” [Int. J. Biochem. Cell Biol. 189 (2025) 106861]","authors":"Meiqi Sun , Hua Fang , Jiashu Zhang , Mengyao Wang , Peng Jiang , LiLi Ma , Huanyu Jin , Wei Zhang","doi":"10.1016/j.biocel.2025.106877","DOIUrl":"10.1016/j.biocel.2025.106877","url":null,"abstract":"","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"189 ","pages":"Article 106877"},"PeriodicalIF":2.8,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145684571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Light-induced retinal damage is a significant contributor to age-related macular degeneration (AMD). Qihuang granule (QHG), a traditional Chinese herbal formulation, has been clinically employed in the treatment of retinal diseases, including AMD; however, the precise protective mechanisms remain unclear. This study investigated the protective effects and underlying mechanisms of QHG using a rat model of blue light-induced retinal injury and a human retinal pigment epithelial (ARPE-19) cell model. The results demonstrated that QHG significantly alleviated retinal morphological abnormalities, ultrastructural damage, and apoptosis induced by light exposure. Single-cell RNA sequencing further revealed that specific cell clusters were notably enriched in the PI3K-AKT-mTOR and autophagy-related signaling pathways after QHG treatment, characterized by increased MAP1LC3B (LC3B) expression and decreased SQSTM1 (P62) expression. Validation at the protein and gene levels in vivo confirmed that QHG activated the autophagy pathway by downregulating PI3K, AKT, mTOR, and P62 expression while upregulating LC3B expression. Collectively, this study demonstrates that QHG protects against retinal photodamage by modulating autophagy via the PI3K/AKT/mTOR signaling pathway, providing theoretical support for its clinical application in the treatment of AMD.
{"title":"Integrative single-cell transcriptomic and experimental analyses unveil Qihuang granule's protection against retinal photodamage via PI3K/AKT/mTOR-mediated autophagy","authors":"Zhao Zhang , Xiaoqian Shan , Fengming Liang , Lulu Fang","doi":"10.1016/j.biocel.2025.106881","DOIUrl":"10.1016/j.biocel.2025.106881","url":null,"abstract":"<div><div>Light-induced retinal damage is a significant contributor to age-related macular degeneration (AMD). Qihuang granule (QHG), a traditional Chinese herbal formulation, has been clinically employed in the treatment of retinal diseases, including AMD; however, the precise protective mechanisms remain unclear. This study investigated the protective effects and underlying mechanisms of QHG using a rat model of blue light-induced retinal injury and a human retinal pigment epithelial (ARPE-19) cell model. The results demonstrated that QHG significantly alleviated retinal morphological abnormalities, ultrastructural damage, and apoptosis induced by light exposure. Single-cell RNA sequencing further revealed that specific cell clusters were notably enriched in the PI3K-AKT-mTOR and autophagy-related signaling pathways after QHG treatment, characterized by increased MAP1LC3B (LC3B) expression and decreased SQSTM1 (P62) expression. Validation at the protein and gene levels in vivo confirmed that QHG activated the autophagy pathway by downregulating PI3K, AKT, mTOR, and P62 expression while upregulating LC3B expression. Collectively, this study demonstrates that QHG protects against retinal photodamage by modulating autophagy via the PI3K/AKT/mTOR signaling pathway, providing theoretical support for its clinical application in the treatment of AMD.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"190 ","pages":"Article 106881"},"PeriodicalIF":2.8,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145624676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-11-18DOI: 10.1016/j.biocel.2025.106879
Yi Wu , Fang Wang , Fang-Lin Peng
Type II diabetes is a prevalent chronic disease worldwide, yet no curative treatment currently exists. Compromised insulin release is one of the hallmarks of type II diabetes, to restore insulin release is one standard to screen candidates for therapy. Proton-activated chloride (PAC) channels are pH-sensitive chloride channels that open under acidic conditions, but their potential role in pancreatic β-cell physiology and diabetes has not been fully explored. In this study, we identified PAC on the membrane of pancreatic β-cells and found it to be closely associated with insulin secretory granules. Immunostaining and FRET imaging revealed that PAC is co-localized with Syntaxin 1 A and CaV1.2. Overexpression and knockdown of PAC increased and reduced L type calcium currents and steady capacitance jumps which reflect fast insulin secretion. Furthermore, manipulation of PAC expression significantly altered overall insulin release under high glucose conditions in vitro. Knockout of PAC channels in mice, however, affects body weight, fasting blood glucose levels, and serum insulin levels when constructing a type II diabetes model through high-fat diet feeding, compared to wild-type mice or Pac knockout mice fed a normal diet. Together, these findings reveal a previously unrecognized role for PAC in regulating both phases of insulin secretion and suggest that PAC channels could represent a novel therapeutic target for improving β-cell function and treating diabetes. Given the global burden of type II diabetes, understanding PAC channel function could open new avenues for targeted interventions to restore insulin secretion and improve disease outcomes.
{"title":"Proton activated chloride channel and its regulation of insulin secretion in β cells","authors":"Yi Wu , Fang Wang , Fang-Lin Peng","doi":"10.1016/j.biocel.2025.106879","DOIUrl":"10.1016/j.biocel.2025.106879","url":null,"abstract":"<div><div>Type II diabetes is a prevalent chronic disease worldwide, yet no curative treatment currently exists. Compromised insulin release is one of the hallmarks of type II diabetes, to restore insulin release is one standard to screen candidates for therapy. Proton-activated chloride (PAC) channels are pH-sensitive chloride channels that open under acidic conditions, but their potential role in pancreatic β-cell physiology and diabetes has not been fully explored. In this study, we identified PAC on the membrane of pancreatic β-cells and found it to be closely associated with insulin secretory granules. Immunostaining and FRET imaging revealed that PAC is co-localized with Syntaxin 1 A and CaV1.2. Overexpression and knockdown of PAC increased and reduced L type calcium currents and steady capacitance jumps which reflect fast insulin secretion. Furthermore, manipulation of PAC expression significantly altered overall insulin release under high glucose conditions in vitro. Knockout of PAC channels in mice, however, affects body weight, fasting blood glucose levels, and serum insulin levels when constructing a type II diabetes model through high-fat diet feeding, compared to wild-type mice or <em>Pac</em> knockout mice fed a normal diet. Together, these findings reveal a previously unrecognized role for PAC in regulating both phases of insulin secretion and suggest that PAC channels could represent a novel therapeutic target for improving β-cell function and treating diabetes. Given the global burden of type II diabetes, understanding PAC channel function could open new avenues for targeted interventions to restore insulin secretion and improve disease outcomes.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"190 ","pages":"Article 106879"},"PeriodicalIF":2.8,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145565775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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