EXPRESSION OF CONCERN: X. Zheng, X. Zhang, L. Dong, J. Zhao, C. Zhang and R. Chen, “Neuroprotective Mechanism of Salvianolic Acid B Against Cerebral Ischemia–Reperfusion Injury in Mice Through Downregulation of TLR4, p-p38MAPK, p-JNK, NF-κB, and IL-1β,” Immunity, Inflammation and Disease 11, no. 10 (2023): e1030, https://doi.org/10.1002/iid3.1030.
This Expression of Concern is for the above article, published online on 04 October 2023 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley & Sons Ltd. The Expression of Concern has been agreed upon due to inconsistencies and discrepancies identified in Figure 2. Although the authors provided some raw data corresponding to the study, the data supplied was incomplete. Additionally, the authors were unable to provide documentation of ethics approval granted prior to the commencement of the study, as required. Instead, retrospective approval was obtained. The journal is issuing this expression of concern to alert readers.
{"title":"EXPRESSION OF CONCERN: Neuroprotective Mechanism of Salvianolic Acid B Against Cerebral Ischemia–Reperfusion Injury in Mice Through Downregulation of TLR4, p-p38MAPK, p-JNK, NF-κB, and IL-1β","authors":"","doi":"10.1002/iid3.70314","DOIUrl":"10.1002/iid3.70314","url":null,"abstract":"<p><b>EXPRESSION OF CONCERN</b>: X. Zheng, X. Zhang, L. Dong, J. Zhao, C. Zhang and R. Chen, “Neuroprotective Mechanism of Salvianolic Acid B Against Cerebral Ischemia–Reperfusion Injury in Mice Through Downregulation of TLR4, p-p38MAPK, p-JNK, NF-κB, and IL-1β,” <i>Immunity, Inflammation and Disease</i> 11, no. 10 (2023): e1030, https://doi.org/10.1002/iid3.1030.</p><p>This Expression of Concern is for the above article, published online on 04 October 2023 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Marc Veldhoen; and John Wiley & Sons Ltd. The Expression of Concern has been agreed upon due to inconsistencies and discrepancies identified in Figure 2. Although the authors provided some raw data corresponding to the study, the data supplied was incomplete. Additionally, the authors were unable to provide documentation of ethics approval granted prior to the commencement of the study, as required. Instead, retrospective approval was obtained. The journal is issuing this expression of concern to alert readers.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12753327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145862976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Zimei Yang, Yimin Wang, Jun Chen, Xinyang Shou, Di Zhang, Zhidong Zhou, Qiang Liu
Objective
Sirtuin 6 (Sirt6) plays a critical role in cardiovascular pathophysiology, yet its involvement in viral myocarditis (VMC) remains poorly understood. This study aimed to investigate the role of Sirt6 in coxsackievirus B3 (CVB3)-induced endothelial-to-mesenchymal transition (EndMT) and its underlying molecular mechanisms.
Methods
A model of CVB3-infected mouse cardiac endothelial cells (MCECs) was established. EndMT markers and Sirt6 expression were detected by WB/IF and qRT-PCR. Lentivirus-mediated Sirt6 knockdown or overexpression was performed to examine its impact on EndMT. Apoptosis and apoptosis-related proteins were analyzed by flow cytometry and WB. Proteomic analysis was further conducted on Sirt6-knockdown MCECs and their controls. Based on the results, oxidative stress and autophagy were assessed in CVB3-induced EndMT, and the influence of altered Sirt6 expression on these indicators was evaluated.
Results
Sirt6 expression was significantly downregulated in CVB3-induced EndMT. Sirt6 knockdown promoted EndMT, as manifested by decreased vascular endothelial cadherin (VE-cad) and increased α-smooth muscle actin (α-SMA) expression. It also exacerbated apoptosis, accompanied by upregulation of pro-apoptotic Bax, downregulation of anti-apoptotic Bcl-2, and an increase in Caspase-3 expression. Sirt6 overexpression partially reversed these changes. Proteomic analysis indicated that Sirt6 was involved in inflammatory signaling, apoptotic cascades, redox homeostasis, and metabolic pathways. CVB3 infection markedly elevated intracellular oxidative stress (increased ROS and MDA levels, decreased SOD activity) and suppressed autophagy (reduced LC3B-II and Beclin-1, elevated p62). These CVB3‑induced effects were aggravated by Sirt6 knockdown but attenuated by Sirt6 overexpression.
Conclusion
This study reveals that Sirt6 inhibits CVB3-induced EndMT by regulating oxidative stress and autophagy. These findings provide experimental evidence for elucidating the pathological mechanisms of VMC and suggest Sirt6 as a potential therapeutic target.
{"title":"Inhibitory Effect of Sirtuin6 on EndMT by Regulating Oxidative Stress and Autophagy in Coxsackievirus B3-Induced Cardiac Endothelial Cells","authors":"Zimei Yang, Yimin Wang, Jun Chen, Xinyang Shou, Di Zhang, Zhidong Zhou, Qiang Liu","doi":"10.1002/iid3.70316","DOIUrl":"10.1002/iid3.70316","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>Sirtuin 6 (Sirt6) plays a critical role in cardiovascular pathophysiology, yet its involvement in viral myocarditis (VMC) remains poorly understood. This study aimed to investigate the role of Sirt6 in coxsackievirus B3 (CVB3)-induced endothelial-to-mesenchymal transition (EndMT) and its underlying molecular mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A model of CVB3-infected mouse cardiac endothelial cells (MCECs) was established. EndMT markers and Sirt6 expression were detected by WB/IF and qRT-PCR. Lentivirus-mediated Sirt6 knockdown or overexpression was performed to examine its impact on EndMT. Apoptosis and apoptosis-related proteins were analyzed by flow cytometry and WB. Proteomic analysis was further conducted on Sirt6-knockdown MCECs and their controls. Based on the results, oxidative stress and autophagy were assessed in CVB3-induced EndMT, and the influence of altered Sirt6 expression on these indicators was evaluated.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Sirt6 expression was significantly downregulated in CVB3-induced EndMT. Sirt6 knockdown promoted EndMT, as manifested by decreased vascular endothelial cadherin (VE-cad) and increased α-smooth muscle actin (α-SMA) expression. It also exacerbated apoptosis, accompanied by upregulation of pro-apoptotic Bax, downregulation of anti-apoptotic Bcl-2, and an increase in Caspase-3 expression. Sirt6 overexpression partially reversed these changes. Proteomic analysis indicated that Sirt6 was involved in inflammatory signaling, apoptotic cascades, redox homeostasis, and metabolic pathways. CVB3 infection markedly elevated intracellular oxidative stress (increased ROS and MDA levels, decreased SOD activity) and suppressed autophagy (reduced LC3B-II and Beclin-1, elevated p62). These CVB3‑induced effects were aggravated by Sirt6 knockdown but attenuated by Sirt6 overexpression.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>This study reveals that Sirt6 inhibits CVB3-induced EndMT by regulating oxidative stress and autophagy. These findings provide experimental evidence for elucidating the pathological mechanisms of VMC and suggest Sirt6 as a potential therapeutic target.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12748517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145855886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kristian Assing, Emil Birch Christensen, Christoffer Dellgren, Kerstin Kathrine Soelberg, Christina Fagerberg, Ida Coordt Elle, Bjørk Ditlev Larsen, Dorthe Grosen, Claire Booth, Hanne Vibeke Marquart, Tania Nicole Masmas, Hans Jakob Hartling
<div> <section> <h3> Objectives</h3> <p>Pathogenic variants in <i>IL2RG</i>, encoding the common γ chain (γ<sub>c</sub>/CD132), usually lead to T − B + NK- X-SCID but can, occasionally, generate a T − B + NK+ phenotype. We wanted to delineate potential mechanisms for this discrepancy.</p> </section> <section> <h3> Methods</h3> <p>The immunological work-up of our patient comprised: whole genome sequencing and subsequent bioinformatics, flow-cytometry (lymphocyte surface receptor expression, STAT5 phosphorylation, NK cell proliferation and degranulation), lymphocyte stimulation (IL-2, IL-4 and IL-15) as well as restriction enzyme digestion and fragment size separation (evaluation of relative WT/variant expression).</p> </section> <section> <h3> Findings</h3> <p>Our patient, hemizygous for a maternally derived, c.677 G > A <i>IL2RG</i> missense variant displayed a T − B + NK+ phenotype, no dysmorphic features and no thymus. The γ<sub>c</sub> was surface expressed. In contrast to B cells from cord-blood and adults (including maternal B cells), only pre-gene therapy (patient) B cells did not decrease IL-4Rα surface expression upon IL-4 stimulation, consistent with compromised IL-4R (and γ<sub>c</sub>) function. After gene therapy, patient B cells decreased IL-4Rα upon Il-4 stimulation. Pre-gene therapy NK cells displayed normal, K562 cell, induced degranulation and, in response to IL-2 and IL-15 and exhibited normal initial pSTAT5 kinetics but clearly attenuated activation and proliferation day six. By restriction enzyme digestion and fragment size separation, selected T and B cells from the healthy mother exhibited skewed expression (92% and 84%, respectively) of the WT <i>IL2RG</i> allele.</p> </section> <section> <h3> Conclusion</h3> <p>The selective WT <i>IL2RG</i> expression in maternal B cells was consistent with the compromised IL-4R signaling (and compromised IL-21R signaling) in her offspring (the patient), as both IL-4 and IL-21 are critical for normal human B cell germinal center reactions but not for peripheral B cell homeostasis. The c.677 G > A <i>IL2RG</i> variant permitted normal NK cell degranulation and initial STAT5 phosphorylation but was incapable of sustaining normal NK cell activation and proliferation in vitro. As IL-2 and IL-15 induced in-vitro NK cell proliferation is primarily mediated through the low affinity βγ<sub>c</sub> (CD122-CD132) complex, our data indicate the importance of high affinity IL-15Rα and IL-2 Rα mediated signaling in-vivo for sustaining NK cell numbers in X-linked SCID. Consequently, we further hypot
目的：IL2RG的致病变异，编码共同γ链（γc/CD132），通常导致T - B + NK- X-SCID，但偶尔也会产生T - B + NK+表型。我们想要描述这种差异的潜在机制。方法：患者的免疫学检查包括：全基因组测序和随后的生物信息学，流式细胞术（淋巴细胞表面受体表达，STAT5磷酸化，NK细胞增殖和脱粒），淋巴细胞刺激（IL-2， IL-4和IL-15）以及限制性内切酶消化和片段大小分离（相对WT/变异表达的评估）。结果：我们的患者是母源性的c.677 G . > a IL2RG错义变异的半合子，表现为T - B + NK+表型，无畸形特征，无胸腺。表面表达γ - c。与脐带血B细胞和成人B细胞（包括母体B细胞）相比，只有基因前治疗（患者）B细胞在IL-4刺激下没有降低IL-4Rα表面表达，这与IL-4R（和γ - c）功能受损一致。基因治疗后，患者B细胞在Il-4刺激下降低IL-4Rα。基因治疗前NK细胞表现为正常的K562细胞，诱导脱颗粒，并对IL-2和IL-15做出反应，并表现出正常的初始pSTAT5动力学，但在第6天明显减弱了激活和增殖。通过限制性内切酶酶切和片段大小分离，来自健康母亲的T细胞和B细胞表现出WT IL2RG等位基因的偏表达（分别为92%和84%）。结论：IL-4和IL-21对正常的人B细胞生发中心反应至关重要，但对外周B细胞稳态不重要。因此，母亲B细胞中选择性WT il - 2rg的表达与其后代（患者）IL-4R信号和IL-21R信号的受损是一致的。c.677 G > A IL2RG变体允许正常NK细胞脱颗粒和初始STAT5磷酸化，但不能维持正常NK细胞的体外活化和增殖。由于IL-2和IL-15诱导的体外NK细胞增殖主要是通过低亲和力的βγc （CD122-CD132）复合物介导的，我们的数据表明，高亲和力的IL-15Rα和il - 2r α介导的体内信号传导对于维持x连锁SCID中NK细胞数量的重要性。因此，我们进一步假设，在x连锁SCID的情况下，即使最初的IL-15和IL-2 STAT5磷酸化被破坏，IL-15（和IL-2）通过高亲和力的IL-15Rα和IL-2Rα受体亚基在体内的转运将无法维持正常的外周NK细胞数量。”
{"title":"Functional Characterization of an IL2RG Variant, a Case Report of X-Linked T- B + NK + SCID","authors":"Kristian Assing, Emil Birch Christensen, Christoffer Dellgren, Kerstin Kathrine Soelberg, Christina Fagerberg, Ida Coordt Elle, Bjørk Ditlev Larsen, Dorthe Grosen, Claire Booth, Hanne Vibeke Marquart, Tania Nicole Masmas, Hans Jakob Hartling","doi":"10.1002/iid3.70307","DOIUrl":"10.1002/iid3.70307","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Pathogenic variants in <i>IL2RG</i>, encoding the common γ chain (γ<sub>c</sub>/CD132), usually lead to T − B + NK- X-SCID but can, occasionally, generate a T − B + NK+ phenotype. We wanted to delineate potential mechanisms for this discrepancy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The immunological work-up of our patient comprised: whole genome sequencing and subsequent bioinformatics, flow-cytometry (lymphocyte surface receptor expression, STAT5 phosphorylation, NK cell proliferation and degranulation), lymphocyte stimulation (IL-2, IL-4 and IL-15) as well as restriction enzyme digestion and fragment size separation (evaluation of relative WT/variant expression).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Findings</h3>\u0000 \u0000 <p>Our patient, hemizygous for a maternally derived, c.677 G > A <i>IL2RG</i> missense variant displayed a T − B + NK+ phenotype, no dysmorphic features and no thymus. The γ<sub>c</sub> was surface expressed. In contrast to B cells from cord-blood and adults (including maternal B cells), only pre-gene therapy (patient) B cells did not decrease IL-4Rα surface expression upon IL-4 stimulation, consistent with compromised IL-4R (and γ<sub>c</sub>) function. After gene therapy, patient B cells decreased IL-4Rα upon Il-4 stimulation. Pre-gene therapy NK cells displayed normal, K562 cell, induced degranulation and, in response to IL-2 and IL-15 and exhibited normal initial pSTAT5 kinetics but clearly attenuated activation and proliferation day six. By restriction enzyme digestion and fragment size separation, selected T and B cells from the healthy mother exhibited skewed expression (92% and 84%, respectively) of the WT <i>IL2RG</i> allele.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The selective WT <i>IL2RG</i> expression in maternal B cells was consistent with the compromised IL-4R signaling (and compromised IL-21R signaling) in her offspring (the patient), as both IL-4 and IL-21 are critical for normal human B cell germinal center reactions but not for peripheral B cell homeostasis. The c.677 G > A <i>IL2RG</i> variant permitted normal NK cell degranulation and initial STAT5 phosphorylation but was incapable of sustaining normal NK cell activation and proliferation in vitro. As IL-2 and IL-15 induced in-vitro NK cell proliferation is primarily mediated through the low affinity βγ<sub>c</sub> (CD122-CD132) complex, our data indicate the importance of high affinity IL-15Rα and IL-2 Rα mediated signaling in-vivo for sustaining NK cell numbers in X-linked SCID. Consequently, we further hypot","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12748512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145855883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study aimed to elucidate the underlying mechanisms by which lipopolysaccharide (LPS) influences differential ovarian responses to controlled ovarian stimulation at the metabolite and gene levels.
Materials and Methods
A total of 16 female mice were randomly allocated into LPS and control group. Each mice underwent controlled ovarian stimulation. Oocytes were gathered and quantified. Ovarian tissue samples from 8 mice and blood samples from 16 mice were collected. Metabolomics analysis was conducted for both ovary tissues and blood samples. Transcriptome sequencing analysis was used for ovary tissues. Spearman's correlation analysis was performed to identify the metabolites and their corresponding differential transcripts genes within the key signaling pathway.
Results
The number (86 vs. 122) and rate (49.7% vs. 78.2%) of metaphase II (MII) oocytes were markedly lower in LPS group (p < 0.001). Compared with control group, metabolites related to carbohydrates and lipid were decreased in ovary tissue of LPS group while metabolites related to amino acid and fatty acid beta-oxidation were decreased in serum of LPS group. Within the category of biological processes, terms associated with the regulation of lipid metabolic process and steroid metabolic, biosynthetic process were downregulated in the LPS group. Correlation analysis indicated five genes (Lcn2, S100a9, S100a8, Muc5b, Muc5ac) in IL-17 signaling pathway were positively related to the catabolites of polyunsaturated fatty acids and negatively related to dihydroxyacetone phosphate.
Conclusions
This study provided evidence that inflammation has damaging effect on ovary response to controlled ovarian stimulation, linked to dysfunctions in lipid, carbohydrate, and amino acid metabolism. IL-17 signal pathways may play a critical role in this process.
{"title":"Integration Analysis of Metabolome and Transcriptome Reveals the Effect of Lipopolysaccharide on Ovary Response to Stimulation","authors":"Xin Mu, Feng Zhu, Yudan Zhang, Mei-Li Pei","doi":"10.1002/iid3.70309","DOIUrl":"10.1002/iid3.70309","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aimed to elucidate the underlying mechanisms by which lipopolysaccharide (LPS) influences differential ovarian responses to controlled ovarian stimulation at the metabolite and gene levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials and Methods</h3>\u0000 \u0000 <p>A total of 16 female mice were randomly allocated into LPS and control group. Each mice underwent controlled ovarian stimulation. Oocytes were gathered and quantified. Ovarian tissue samples from 8 mice and blood samples from 16 mice were collected. Metabolomics analysis was conducted for both ovary tissues and blood samples. Transcriptome sequencing analysis was used for ovary tissues. Spearman's correlation analysis was performed to identify the metabolites and their corresponding differential transcripts genes within the key signaling pathway.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The number (86 vs. 122) and rate (49.7% vs. 78.2%) of metaphase II (MII) oocytes were markedly lower in LPS group (<i>p</i> < 0.001). Compared with control group, metabolites related to carbohydrates and lipid were decreased in ovary tissue of LPS group while metabolites related to amino acid and fatty acid beta-oxidation were decreased in serum of LPS group. Within the category of biological processes, terms associated with the regulation of lipid metabolic process and steroid metabolic, biosynthetic process were downregulated in the LPS group. Correlation analysis indicated five genes (Lcn2, S100a9, S100a8, Muc5b, Muc5ac) in IL-17 signaling pathway were positively related to the catabolites of polyunsaturated fatty acids and negatively related to dihydroxyacetone phosphate.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study provided evidence that inflammation has damaging effect on ovary response to controlled ovarian stimulation, linked to dysfunctions in lipid, carbohydrate, and amino acid metabolism. IL-17 signal pathways may play a critical role in this process.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12728487/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145819146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J. Lu, B. Gu, W. Lu, J. Liu, and J. Lu, “Lnc-ANRIL Modulates the Immune Response Associated With NF-κB Pathway in LPS-Stimulated Bovine Mammary Epithelial Cells.” Immunity, Inflammation and Disease 11, no. 12 (2023): e1125, https://doi.org/10.1002/iid3.1125.
In Figure 4B of this paper, the Caspase-3 bands were mistakenly duplicated from the P27 bands shown in Figure 3B. The authors have provided the original image for the Caspase-3 bands and corrected the figure. They confirm that all experimental results and corresponding conclusions in the paper remain unaffected. The corrected Caspase-3 bands and the updated Figure 4 are shown below.
{"title":"Correction to “Lnc-ANRIL Modulates the Immune Response Associated With NF-κB Pathway in LPS-Stimulated Bovine Mammary Epithelial Cells”","authors":"","doi":"10.1002/iid3.70308","DOIUrl":"10.1002/iid3.70308","url":null,"abstract":"<p>J. Lu, B. Gu, W. Lu, J. Liu, and J. Lu, “Lnc-ANRIL Modulates the Immune Response Associated With NF-κB Pathway in LPS-Stimulated Bovine Mammary Epithelial Cells.” <i>Immunity, Inflammation and Disease</i> 11, no. 12 (2023): e1125, https://doi.org/10.1002/iid3.1125.</p><p>In Figure 4B of this paper, the Caspase-3 bands were mistakenly duplicated from the P27 bands shown in Figure 3B. The authors have provided the original image for the Caspase-3 bands and corrected the figure. They confirm that all experimental results and corresponding conclusions in the paper remain unaffected. The corrected Caspase-3 bands and the updated Figure 4 are shown below.</p><p>Corrected caspase - 3 bands</p><p>Corrected Figure 4</p><p>The authors apologize for this error.</p>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70308","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145774215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cordyceps sinensis (CS) is a fungus that parasitizes the larvae and corpses of Batmadaceae insects. CS is used as a traditional Chinese medicine and has shown promising clinical efficacy in the treatment of chronic obstructive pulmonary disease (COPD). This study aimed to identify potential targets of CS in the treatment of COPD and to analyse the related biological processes and signalling pathways.
Methods
Through the use of network pharmacological tools, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, as well as corroborating data from Gene Expression Omnibus (GEO) and the literature, potential targets for CS treatment of COPD were identified and analysed.
Results
These results suggest that CS alleviates COPD symptoms with key biomarkers such as interleukins (ILs), tumour necrosis factor (TNF), and reactive oxygen species (ROS). The primary active constituents of CS comprise Cordycepin, D-mannitol, Ergosterol, Cordyceps polysaccharides, and others. During the pathogenesis of COPD, CS exerts modulates effects on various proteins and signalling pathways, influencing gene expression patterns such as poly ADP-ribose polymerase 1 (PARP1), phosphodiesterase 4A (PDE4A), phosphodiesterase 4B (PDE4B), phosphodiesterase 4C (PDE4C), phosphodiesterase 4D (PDE4D), prostaglandin D2 receptor 2 (PTGDR2), heme oxygenase 1 (HMOX1), and matrix metallopeptidase 1 (MMP1).
Conclusion
CS alleviates COPD symptoms by suppressing inflammation, apoptosis, and oxidative stress, suggesting novel therapeutic strategies.
{"title":"Cordyceps sinensis (CS) Alleviates Chronic Obstructive Pulmonary Disease Symptoms (COPD) by Targeting Inflammation, Apoptosis, and Oxidative Stress Through Ingredient–Gene–Disease Interaction","authors":"Zirui Zang, Yuhan Kong, Qi Kong","doi":"10.1002/iid3.70306","DOIUrl":"10.1002/iid3.70306","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p><i>Cordyceps sinensis</i> (CS) is a fungus that parasitizes the larvae and corpses of Batmadaceae insects. CS is used as a traditional Chinese medicine and has shown promising clinical efficacy in the treatment of chronic obstructive pulmonary disease (COPD). This study aimed to identify potential targets of CS in the treatment of COPD and to analyse the related biological processes and signalling pathways.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Through the use of network pharmacological tools, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, as well as corroborating data from Gene Expression Omnibus (GEO) and the literature, potential targets for CS treatment of COPD were identified and analysed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>These results suggest that CS alleviates COPD symptoms with key biomarkers such as interleukins (ILs), tumour necrosis factor (TNF), and reactive oxygen species (ROS). The primary active constituents of CS comprise Cordycepin, <span>D</span>-mannitol, Ergosterol, Cordyceps polysaccharides, and others. During the pathogenesis of COPD, CS exerts modulates effects on various proteins and signalling pathways, influencing gene expression patterns such as poly ADP-ribose polymerase 1 (PARP1), phosphodiesterase 4A (PDE4A), phosphodiesterase 4B (PDE4B), phosphodiesterase 4C (PDE4C), phosphodiesterase 4D (PDE4D), prostaglandin D2 receptor 2 (PTGDR2), heme oxygenase 1 (HMOX1), and matrix metallopeptidase 1 (MMP1).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>CS alleviates COPD symptoms by suppressing inflammation, apoptosis, and oxidative stress, suggesting novel therapeutic strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12705339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145762577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Åsa Andersson, M. Charlotte Olsson, Anna Torell, Elisabeth Mogard, Emma Haglund
Background
Axial spondyloarthritis (axSpA) is a chronic inflammatory disease primarily affecting the axial skeleton causing pain, inflammation, and stiffness. Individuals with axSpA are at greater risk of developing cardiovascular disease, which can be counteracted by physical activity. High-intensity interval training (HIIT) has been shown to improve cardiovascular health, but the effect on disease activity and the level of inflammation in axSpA has been less studied. In the herein presented pilot study, the aim was to investigate if serum levels of inflammatory cytokines, myokines, and protein markers for bone metabolism are acutely affected by one bout of HIIT in individuals with axSpA and healthy controls (HC).
Methods
Ten participants with axSpA (medication: 6 NSAIDs, 3 biologics, 1 no-treatment) and 11 age- and sex-matched HC performed a single HIIT bout on a cycle ergometer: 4 × 4 min intervals with 3 min active rest in between. Blood samples were taken before and 1 h after the HIIT bout. Serum proteins (IL-6, IL-17, IL-18, TNF-α, CXCL-10, VEGF-A, BDNF, DKK-1, osteoprotegerin, osteocalcin, osteopontin, BMP-7, CRP) were analyzed with a Luminex system or ELISA. A two-way ANOVA was used for comparisons.
Results
A main effect from baseline to 1 h post HIIT showed that both groups had a significant increase in serum levels of IL-6. VEGF-A was significantly lower in the axSpA group but was not affected by the HIIT bout. BMP-7 increased in both groups after the HIIT. For the other proteins analyzed, there were no significant differences in serum concentrations between individuals with axSpA and HC, or within the two groups before and after one bout of HIIT.
Conclusions
One acute bout of HIIT significantly increases the serum concentrations of IL-6 and BMP-7 after 1 h in both individuals with axSpA and HC, whereas serum levels of other proteins investigated are not changed.
{"title":"Effects on Serum Protein Levels From One Bout of High Intensity Interval Training in Individuals With Axial Spondyloarthritis and Controls","authors":"Åsa Andersson, M. Charlotte Olsson, Anna Torell, Elisabeth Mogard, Emma Haglund","doi":"10.1002/iid3.70305","DOIUrl":"https://doi.org/10.1002/iid3.70305","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Axial spondyloarthritis (axSpA) is a chronic inflammatory disease primarily affecting the axial skeleton causing pain, inflammation, and stiffness. Individuals with axSpA are at greater risk of developing cardiovascular disease, which can be counteracted by physical activity. High-intensity interval training (HIIT) has been shown to improve cardiovascular health, but the effect on disease activity and the level of inflammation in axSpA has been less studied. In the herein presented pilot study, the aim was to investigate if serum levels of inflammatory cytokines, myokines, and protein markers for bone metabolism are acutely affected by one bout of HIIT in individuals with axSpA and healthy controls (HC).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Ten participants with axSpA (medication: 6 NSAIDs, 3 biologics, 1 no-treatment) and 11 age- and sex-matched HC performed a single HIIT bout on a cycle ergometer: 4 × 4 min intervals with 3 min active rest in between. Blood samples were taken before and 1 h after the HIIT bout. Serum proteins (IL-6, IL-17, IL-18, TNF-α, CXCL-10, VEGF-A, BDNF, DKK-1, osteoprotegerin, osteocalcin, osteopontin, BMP-7, CRP) were analyzed with a Luminex system or ELISA. A two-way ANOVA was used for comparisons.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A main effect from baseline to 1 h post HIIT showed that both groups had a significant increase in serum levels of IL-6. VEGF-A was significantly lower in the axSpA group but was not affected by the HIIT bout. BMP-7 increased in both groups after the HIIT. For the other proteins analyzed, there were no significant differences in serum concentrations between individuals with axSpA and HC, or within the two groups before and after one bout of HIIT.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>One acute bout of HIIT significantly increases the serum concentrations of IL-6 and BMP-7 after 1 h in both individuals with axSpA and HC, whereas serum levels of other proteins investigated are not changed.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 12","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70305","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145750854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Li-Yang Zhang, Chun-Hui She, Hu Dan, Jun Zou, Jian-Long Guan
Objectives
Behçet's syndrome (BS) is a rare inflammatory disorder with life-threatening complications like myocardial infarction (MI), driven by vasculitis and immune-mediated thrombosis. This study unveils distinct clinical and molecular profiles in BS patients with MI, employing gene analysis and Weighted Gene Co-expression Network Analysis (WGCNA) to pinpoint critical pathways and therapeutic targets, enhancing diagnostic precision and treatment efficacy.
Methods
A total of 2358 BS patients (25 with MI, 2333 without MI) were analyzed. Clinical characteristics were compared based on the cohort. Differential gene expression analysis was performed on four microarray datasets, by using GEO datasets, and WGCNA identified key gene modules. KEGG/GO enrichment revealed disease pathways, while diagnostic models (ROC curves, nomograms) evaluated predictive accuracy.
Results
BS patients with MI exhibited longer disease duration, higher smoking rates, and increased vascular and cardiac involvement. Gene analysis identified 605 BS- and 523 MI-related genes, with pathways linked to immune regulation and vascular remodeling. Three genes, TLR5, IL2RB, and KLRB1, showed strong diagnostic potential (AUC > 0.8). A nomogram integrating these genes achieved high predictive accuracy (AUC = 0.876).
Conclusions
This study reveals distinct clinical and molecular profiles in BS-associated MI, emphasizing inflammatory pathways and immune dysregulation. The findings provide a foundation for early diagnosis and personalized therapeutic strategies, advancing care for BS patients at risk for MI.
{"title":"Unraveling the Clinical and Molecular Landscape of Myocardial Infarction in Behçet's Syndrome: A Comprehensive Analysis","authors":"Li-Yang Zhang, Chun-Hui She, Hu Dan, Jun Zou, Jian-Long Guan","doi":"10.1002/iid3.70303","DOIUrl":"https://doi.org/10.1002/iid3.70303","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>Behçet's syndrome (BS) is a rare inflammatory disorder with life-threatening complications like myocardial infarction (MI), driven by vasculitis and immune-mediated thrombosis. This study unveils distinct clinical and molecular profiles in BS patients with MI, employing gene analysis and Weighted Gene Co-expression Network Analysis (WGCNA) to pinpoint critical pathways and therapeutic targets, enhancing diagnostic precision and treatment efficacy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A total of 2358 BS patients (25 with MI, 2333 without MI) were analyzed. Clinical characteristics were compared based on the cohort. Differential gene expression analysis was performed on four microarray datasets, by using GEO datasets, and WGCNA identified key gene modules. KEGG/GO enrichment revealed disease pathways, while diagnostic models (ROC curves, nomograms) evaluated predictive accuracy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>BS patients with MI exhibited longer disease duration, higher smoking rates, and increased vascular and cardiac involvement. Gene analysis identified 605 BS- and 523 MI-related genes, with pathways linked to immune regulation and vascular remodeling. Three genes, TLR5, IL2RB, and KLRB1, showed strong diagnostic potential (AUC > 0.8). A nomogram integrating these genes achieved high predictive accuracy (AUC = 0.876).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>This study reveals distinct clinical and molecular profiles in BS-associated MI, emphasizing inflammatory pathways and immune dysregulation. The findings provide a foundation for early diagnosis and personalized therapeutic strategies, advancing care for BS patients at risk for MI.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 11","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70303","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145626347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Human Leukocyte Antigen (HLA) compatibility is a key driver of kidney allograft outcomes, yet how matching interacts with immunosuppressant dosing remains unclear. This study evaluates whether low-resolution HLA match fractions affect mean dosing and quantified the joint impact of match quality and dose on rejection risk.
Methods
In 519 transplants grouped by HLA match (0–1.0 in 7 strata), full data completeness and variance homogeneity is confirmed, followed by the usage of one-way ANOVA to compare mean doses. Ridge-penalized logistic regression models was fitted at each match level to predict rejection probability across low- and high-dose regimens, deriving absolute and relative risk reductions.
Results
ANOVA showed no significant dosing differences by match (F6,512 = 0.93, p = 0.47). Logistic models revealed that Absolute Risk Reduction rose from ~0.75% at zero match to ~1.25% at perfect match, while mid-range match groups (0.2–0.6) yielded the highest total prevented rejections under high-dose therapy.
Conclusion
Uniform baseline dosing eliminates bias, allowing clear attribution of benefit to immunologic compatibility. These findings endorse a risk-tailored immunosuppression approach intensifying doses where match is low and potentially reducing them in highly compatible transplants and identify match ranges that maximize rejection prevention.
人类白细胞抗原（HLA）相容性是肾移植结果的关键驱动因素，但配型如何与免疫抑制剂剂量相互作用仍不清楚。本研究评估低分辨率HLA匹配分数是否影响平均剂量，并量化匹配质量和剂量对排斥风险的共同影响。方法将519例移植患者按HLA配型（0 ~ 1.0分7层）分组，证实数据完全完整，方差齐性，采用单因素方差分析比较平均剂量。在每个匹配水平上拟合脊惩罚逻辑回归模型，以预测低剂量和高剂量方案的排斥概率，得出绝对和相对风险降低。结果方差分析显示，配对后剂量差异无统计学意义（F6,512 = 0.93, p = 0.47）。Logistic模型显示，绝对风险降低率从零匹配时的0.75%上升到完全匹配时的1.25%，而中等匹配组（0.2-0.6）在高剂量治疗下产生了最高的总预防排斥反应。结论：统一的基线剂量消除了偏倚，明确了免疫相容性带来的益处。这些发现支持一种风险定制的免疫抑制方法，在匹配度低的地方增加剂量，并可能在高度相容的移植中减少剂量，并确定匹配范围，最大限度地预防排斥反应。
{"title":"Immunosuppression Efficacy via Nonlinear Modeling and Probabilistic Analysis of Human Leukocyte Antigen Match and Dose Effects on Allograft Rejection Risk","authors":"Samrajya Raj Acharya, Aayush Man Regmi, Sushil Ghimire, Ram Prasad Ghimire","doi":"10.1002/iid3.70302","DOIUrl":"https://doi.org/10.1002/iid3.70302","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Human Leukocyte Antigen (HLA) compatibility is a key driver of kidney allograft outcomes, yet how matching interacts with immunosuppressant dosing remains unclear. This study evaluates whether low-resolution HLA match fractions affect mean dosing and quantified the joint impact of match quality and dose on rejection risk.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In 519 transplants grouped by HLA match (0–1.0 in 7 strata), full data completeness and variance homogeneity is confirmed, followed by the usage of one-way ANOVA to compare mean doses. Ridge-penalized logistic regression models was fitted at each match level to predict rejection probability across low- and high-dose regimens, deriving absolute and relative risk reductions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>ANOVA showed no significant dosing differences by match (<i>F</i><sub>6,512</sub> = 0.93, <i>p</i> = 0.47). Logistic models revealed that Absolute Risk Reduction rose from ~0.75% at zero match to ~1.25% at perfect match, while mid-range match groups (0.2–0.6) yielded the highest total prevented rejections under high-dose therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Uniform baseline dosing eliminates bias, allowing clear attribution of benefit to immunologic compatibility. These findings endorse a risk-tailored immunosuppression approach intensifying doses where match is low and potentially reducing them in highly compatible transplants and identify match ranges that maximize rejection prevention.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 11","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70302","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145626649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
ROS are pivotal in maintaining periodontal tissue health due to their dual role in physiological and pathological states. At physiological levels, ROS are essential for host defense, effectively eliminating pathogenic bacteria during inflammation and sustaining the homeostasis of the periodontal microenvironment. However, excessive ROS production disrupts the balance between oxidative activity and antioxidant defenses, leading to oxidative stress (OS). This imbalance exacerbates inflammation, damages cellular components, and drives periodontal tissue destruction. Recognizing the dual role of ROS underscores the importance of studying their regulatory mechanisms, which is crucial for advancing understanding and therapeutic strategies in periodontitis management.
Objective
This review summarizes the latest research advancements on the molecular mechanisms linking ROS to the progression of periodontitis and explores related therapeutic strategies.
Results
This review focuses on the pivotal role and specific mechanisms of periodontal tissue destruction by excess ROS, which mediate signaling pathways such as nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK), as well as the activation of OS response-associated proteins, including thioredoxin-interacting protein (TXNIP) and mitochondrial antiviral signaling protein (MAVS). Additionally, we provide a concise summary of emerging therapeutic strategies for periodontitis, including the use of antioxidants, photodynamic therapy (PDT), and nanomaterials. Gaining a more profound comprehension of these mechanisms may pave the way for the formulation of enhanced therapeutic strategies for periodontitis.
Conclusion
Understanding the interplay between ROS and periodontal tissue destruction is essential for advancing periodontitis research. Targeting the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome with antioxidant and ROS-modulating therapies presents a promising strategy to mitigate both inflammation and OS, thereby reducing periodontal degradation.
{"title":"The Role of Reactive Oxygen Species (ROS) in Periodontitis: A Potential Therapeutic Target","authors":"Shuyu Yang, Xi Yang","doi":"10.1002/iid3.70301","DOIUrl":"https://doi.org/10.1002/iid3.70301","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>ROS are pivotal in maintaining periodontal tissue health due to their dual role in physiological and pathological states. At physiological levels, ROS are essential for host defense, effectively eliminating pathogenic bacteria during inflammation and sustaining the homeostasis of the periodontal microenvironment. However, excessive ROS production disrupts the balance between oxidative activity and antioxidant defenses, leading to oxidative stress (OS). This imbalance exacerbates inflammation, damages cellular components, and drives periodontal tissue destruction. Recognizing the dual role of ROS underscores the importance of studying their regulatory mechanisms, which is crucial for advancing understanding and therapeutic strategies in periodontitis management.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This review summarizes the latest research advancements on the molecular mechanisms linking ROS to the progression of periodontitis and explores related therapeutic strategies.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>This review focuses on the pivotal role and specific mechanisms of periodontal tissue destruction by excess ROS, which mediate signaling pathways such as nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK), as well as the activation of OS response-associated proteins, including thioredoxin-interacting protein (TXNIP) and mitochondrial antiviral signaling protein (MAVS). Additionally, we provide a concise summary of emerging therapeutic strategies for periodontitis, including the use of antioxidants, photodynamic therapy (PDT), and nanomaterials. Gaining a more profound comprehension of these mechanisms may pave the way for the formulation of enhanced therapeutic strategies for periodontitis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Understanding the interplay between ROS and periodontal tissue destruction is essential for advancing periodontitis research. Targeting the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome with antioxidant and ROS-modulating therapies presents a promising strategy to mitigate both inflammation and OS, thereby reducing periodontal degradation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":13289,"journal":{"name":"Immunity, Inflammation and Disease","volume":"13 11","pages":""},"PeriodicalIF":2.7,"publicationDate":"2025-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iid3.70301","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145626163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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