IF 14.1

MedComm Pub Date : 2026-09-16 DOI: 10.1002/mco2.71003

Guolin Miao, Zhaoling Li, Lianxin Zhang, Yitong Xu, Ziwei Wang, Zixun Wang, Aiden Xian, Liwen Zheng, Jingxuan Chen, Yufei Han, Chunhua Shan, Kaikai Lu, Ming Tao, Ling Zhang, Weiguang Zhang, Wei Huang, Yuhui Wang, Rui Wei, Erdan Dong, Xunde Xian

{"title":"Adipocyte-Derived KIF13B Aggravates Obesity-Associated Metabolic Dysfunction via LRP1/PPARγ Signaling","authors":"Guolin Miao, Zhaoling Li, Lianxin Zhang, Yitong Xu, Ziwei Wang, Zixun Wang, Aiden Xian, Liwen Zheng, Jingxuan Chen, Yufei Han, Chunhua Shan, Kaikai Lu, Ming Tao, Ling Zhang, Weiguang Zhang, Wei Huang, Yuhui Wang, Rui Wei, Erdan Dong, Xunde Xian","doi":"10.1002/mco2.71003","DOIUrl":"10.1002/mco2.71003","url":null,"abstract":"Obesity is driven by maladaptive adipose expansion, yet the intracellular machinery linking motor protein-associated intracellular regulation to adipogenic transcription remains incompletely understood. Here, we identify adipocyte-derived kinesin family member 13B (KIF13B) as a regulator of obesity-associated metabolic dysfunction through lipoprotein receptor-related protein 1 (LRP1)/peroxisome proliferator-activated receptor γ (PPARγ) signaling. KIF13B expression is markedly upregulated in adipose tissue from humans and mice with obesity. Adipocyte-specific Kif13b deletion protected mice from high-fat diet-induced weight gain, adipose expansion and inflammation, dyslipidemia, insulin resistance, and hepatic steatosis, while promoting thermogenic remodeling. In mice with established diet-induced obesity, adeno-associated virus serotype 9 (AAV9)-mediated adipocyte-targeted KIF13B knockdown improved adipose inflammation, lipid and glucose homeostasis, and liver injury; selected metabolic benefits were also observed in ob/ob mice. Mechanistically, KIF13B facilitates PPARγ-responsive transcriptional activity and adipogenic lipid accumulation via LRP1. This proadipogenic KIF13B/LRP1/PPARγ axis is further supported by human adipose transcriptomic analyses, which reveal positive correlations among its components in obesity and Type 2 diabetes. These findings define a previously unrecognized KIF13B–LRP1–PPARγ axis linking intracellular trafficking to pathological adipocyte remodeling and support adipocyte KIF13B as a potential therapeutic target for obesity-associated metabolic disease.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13583444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148993283","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}

引用次数: 0

Improvements With Tiotropium Maintenance Therapy in COPD Patients Without Dyspnea 噻托溴铵维持治疗对无呼吸困难COPD患者的改善作用。

IF 14.1

MedComm Pub Date : 2026-09-16 DOI: 10.1002/mco2.71001

Zihui Wang, Junfeng Lin, Guannan Cai, Fan Wu, Zhishan Deng, Qi Wan, Gaoying Tang, Cuiqiong Dai, Lifei Lu, Kunning Zhou, Xiaohui Wu, Suyin Huang, Fangyan Wu, Nanshan Zhong, Yumin Zhou, Pixin Ran

{"title":"Improvements With Tiotropium Maintenance Therapy in COPD Patients Without Dyspnea","authors":"Zihui Wang, Junfeng Lin, Guannan Cai, Fan Wu, Zhishan Deng, Qi Wan, Gaoying Tang, Cuiqiong Dai, Lifei Lu, Kunning Zhou, Xiaohui Wu, Suyin Huang, Fangyan Wu, Nanshan Zhong, Yumin Zhou, Pixin Ran","doi":"10.1002/mco2.71001","DOIUrl":"10.1002/mco2.71001","url":null,"abstract":"Current Global Initiative for Chronic Obstructive Lung Disease (GOLD) recommendations emphasize symptom-driven management, which may limit the use of maintenance bronchodilator therapy in patients without dyspnea. In this exploratory post hoc analysis of the tiotropium in early-stage chronic obstructive pulmonary disease (Tie-COPD) trial, we assessed tiotropium in 305 patients with mild-to-moderate chronic obstructive pulmonary disease (COPD) and a modified Medical Research Council dyspnea score of 0 (157 tiotropium, 148 placebo). Over 2 years, tiotropium maintained a higher pre-bronchodilator forced expiratory volume in 1 s (FEV1) than placebo (adjusted between-group differences 143–183 mL; all p < 0.001). The lung function benefit was similar across subgroups defined by age, body mass index, symptom burden, blood eosinophil count, GOLD stage, and smoking (all p for interaction >0.05). The annual exacerbation rate was lower with tiotropium (adjusted incidence rate ratio 0.51, 95% confidence interval [CI] 0.32, 0.82; p = 0.005), as was the risk of a first clinically important deterioration (adjusted hazard ratio 0.55, 95% CI 0.43, 0.70; p < 0.001), whereas COPD assessment test and clinical COPD questionnaire scores did not differ. These hypothesis-generating findings indicate that tiotropium may provide benefits in lung function and exacerbations in COPD without dyspnea, suggesting that a strictly symptom-based treatment criterion warrants prospective reevaluation.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13583477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148993289","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}

引用次数: 0

Genetic Regulation of DNA Methylation and Its Mediating Role in Blood Pressure: A Genome-Wide Twin Study DNA甲基化的遗传调控及其在血压中的介导作用：一项全基因组双胞胎研究。

IF 14.1

MedComm Pub Date : 2026-09-16 DOI: 10.1002/mco2.71004

Xuanming Hong, Ming Li, Weihua Cao, Jun Lv, Canqing Yu, Tao Huang, Dianjianyi Sun, Chunxiao Liao, Yuanjie Pang, Runhua Hu, Ruqin Gao, Min Yu, Jinyi Zhou, Xianping Wu, Yu Liu, Shengli Yin, Wenjing Gao, Liming Li

{"title":"Genetic Regulation of DNA Methylation and Its Mediating Role in Blood Pressure: A Genome-Wide Twin Study","authors":"Xuanming Hong, Ming Li, Weihua Cao, Jun Lv, Canqing Yu, Tao Huang, Dianjianyi Sun, Chunxiao Liao, Yuanjie Pang, Runhua Hu, Ruqin Gao, Min Yu, Jinyi Zhou, Xianping Wu, Yu Liu, Shengli Yin, Wenjing Gao, Liming Li","doi":"10.1002/mco2.71004","DOIUrl":"10.1002/mco2.71004","url":null,"abstract":"DNA methylation regulates gene expression, yet its role in the genetic regulation of blood pressure (BP) remains unclear. Using 1056 Chinese National Twin Registry participants (528 twin pairs), we estimated genome-wide DNA methylation heritability and genetic correlations between DNA methylation and BP using structural equation models. Genetically correlated CpGs were then tested using linear mixed-effects models in the full sample and in monozygotic twin pairs. Mendelian randomization (MR) was applied using East Asian methylation quantitative trait locus (mQTL) and genome-wide association study (GWAS) data, followed by integration of cis-expression QTL and cis-protein QTL data and MR-based mediation analysis to examine whether upstream genes and proteins influence BP through DNA methylation. Genome-wide DNA methylation heritability averaged 18.3%, with modest genetic correlations between DNA methylation and BP (mean |rA| = 0.08–0.09). Association analyses identified 914 and 624 CpGs for systolic and diastolic BP, respectively, with substantial attenuation in monozygotic within-pair analyses, suggesting predominant genetic influences. Bidirectional relationships were identified between six CpGs and BP. MR-based mediation estimates suggested that methylation at specific sites may mediate 34%–93% of upstream gene/protein effects on BP, implicating HBEGF, CARD9, XCL1, and PCOLCE. These findings highlight DNA methylation as a potentially important regulatory layer in genetically influenced BP pathways.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13583443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148993313","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}

引用次数: 0

Mesenchymal Stem Cell-Derived Extracellular Vesicles Ameliorate NaIO3-Induced Dry AMD by Delivering miR-486-3p to Inhibit Lipocalin-2-Mediated Ferroptosis 间充质干细胞来源的细胞外囊泡通过递送miR-486-3p抑制lipocalin -2介导的铁凋亡改善naio3诱导的干性AMD

IF 14.1

MedComm Pub Date : 2026-09-16 DOI: 10.1002/mco2.71000

Zheng Li, Tujing Zhao, Lin Ye, Runze Li, Huaping Tian, Ruilin Liao, Lulin Huang

{"title":"Mesenchymal Stem Cell-Derived Extracellular Vesicles Ameliorate NaIO3-Induced Dry AMD by Delivering miR-486-3p to Inhibit Lipocalin-2-Mediated Ferroptosis","authors":"Zheng Li, Tujing Zhao, Lin Ye, Runze Li, Huaping Tian, Ruilin Liao, Lulin Huang","doi":"10.1002/mco2.71000","DOIUrl":"10.1002/mco2.71000","url":null,"abstract":"Dry age-related macular degeneration (AMD), affecting over 196 million people globally, represents the leading cause of irreversible blindness with limited disease-modifying therapies. The disease is characterized by progressive retinal pigment epithelium (RPE) degeneration driven by ferroptosis, an iron-dependent form of regulated cell death. While mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) show therapeutic promise, their mechanisms in counteracting RPE ferroptosis remain unexplored. Here, we prove that human umbilical cord MSC-derived EVs (hucMSC-EVs) significantly attenuate NaIO3-induced retinal degeneration, preserving retinal structure and improving visual function in mice. Transcriptomic profiling identified Lipocalin-2 (Lcn2) as a key ferroptosis-related target. MSC-EVs administration markedly downregulated Lcn2 and upregulated Gpx4 in NaIO3-induced models, demonstrating potent ferroptosis suppression. Furthermore, AAV-mediated Lcn2 overexpression induced AMD-like retinal pathology, which was effectively attenuated by subsequent MSC-EVs treatment. Small RNA sequencing reveals miR-486-3p as the key factor in the MSC-EVs, and dual-luciferase reporter assays confirm its direct binding to the Lcn2 3'UTR. Functional validation demonstrates that miR-486-3p agomir recapitulates the effects of MSC-EVs, including preservation of retinal structure and improvement of electrophysiological responses. Our findings establish a novel strategy where hucMSC-EVs deliver miR-486-3p to suppress Lcn2-mediated ferroptosis, offering a potential treatment for dry AMD.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13583448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148993272","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}

引用次数: 0

Dynamic Changes of Neutrophil Nuclear Membrane CD63 as a Potential Biomarker for Early Adjunctive Diagnosis and Prognostic Evaluation of Sepsis in Critically Ill Patients: A Prospective Cohort Study 中性粒细胞核膜CD63作为危重症患者早期辅助诊断和预后评估的潜在生物标志物的动态变化：一项前瞻性队列研究

IF 14.1

MedComm Pub Date : 2026-09-16 DOI: 10.1002/mco2.71007

Xingxin Gao, Min Zhang, Linbin Li, Haihua Lyu, Zhihao Liu, Xucheng Wei, Dehui Li, Yiming Shao

{"title":"Dynamic Changes of Neutrophil Nuclear Membrane CD63 as a Potential Biomarker for Early Adjunctive Diagnosis and Prognostic Evaluation of Sepsis in Critically Ill Patients: A Prospective Cohort Study","authors":"Xingxin Gao, Min Zhang, Linbin Li, Haihua Lyu, Zhihao Liu, Xucheng Wei, Dehui Li, Yiming Shao","doi":"10.1002/mco2.71007","DOIUrl":"10.1002/mco2.71007","url":null,"abstract":"Sepsis has high intensive care unit mortality because biomarkers for early reversible pathological events are lacking. Targeted nuclear degranulation, the rate-limiting step in neutrophil extracellular trap formation, refers to azurophilic granule fusion with the nuclear membrane. As an exclusive granule membrane marker, CD63 enrichment in nuclear membranes directly reflects this early pathogenic process. We developed a flow cytometry assay to quantify nuclear membrane CD63 (nmCD63) and validated its clinical utility in a two-center prospective cohort with strict independent external validation. Assay protocols, diagnostic cutoffs, and combined models were established for the derivation cohort (n = 180) and applied without recalibration to the validation cohort (n = 76) comprising 256 participants. nmCD63 levels increased progressively with disease severity. They differentiated non-infectious systemic inflammation from non-severe infections (area under the curve [AUC] = 0.794) and outperformed C-reactive protein and procalcitonin levels. Combined with the Sequential Organ Failure Assessment score, nmCD63 achieved an AUC of 0.943 for identifying sepsis in patients with a confirmed infection. Dynamic nmCD63 shifts preceded changes in all conventional biomarkers, and 7-day trajectories enabled reliable prognostic stratification. This study translates targeted nuclear degranulation as a practical biomarker with dual diagnostic and prognostic value for sepsis in critically ill patients.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13583469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148993357","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}

引用次数: 0

Inhibition of COX-2-Mediated Arachidonic Acid Metabolism by FGF21-PPARα Axis Alleviates Liver Steatosis FGF21-PPARα轴抑制cox -2介导的花生四烯酸代谢减轻肝脏脂肪变性

IF 14.1

MedComm Pub Date : 2026-09-15 DOI: 10.1002/mco2.70999

Guangsen Xu, Tingting Pan, Guiyun Wang, Feng Qiu, Junlin Leng, Qiyang Feng, Yongguo Xue, Ye Wang, Junwei Zheng, Huiying Lu, Bingyan Han, Suntao Wang, Jie Du, Jiaojian Lv, Baile Wang, Xuebo Pan

{"title":"Inhibition of COX-2-Mediated Arachidonic Acid Metabolism by FGF21-PPARα Axis Alleviates Liver Steatosis","authors":"Guangsen Xu, Tingting Pan, Guiyun Wang, Feng Qiu, Junlin Leng, Qiyang Feng, Yongguo Xue, Ye Wang, Junwei Zheng, Huiying Lu, Bingyan Han, Suntao Wang, Jie Du, Jiaojian Lv, Baile Wang, Xuebo Pan","doi":"10.1002/mco2.70999","DOIUrl":"https://doi.org/10.1002/mco2.70999","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) is associated with disturbances in arachidonic acid (AA) metabolism; however, the role and regulation of cyclooxygenase-2 (COX-2), a key enzyme in AA metabolism, during disease progression remain incompletely understood. Here, we identify fibroblast growth factor 21 (FGF21) as a previously unrecognized suppressor of hepatic COX-2 in MASLD. Although both FGF21 and COX-2 were elevated in steatotic livers, FGF21 deficiency further augmented hepatic COX-2 expression in mice fed with a high-fat diet, leading to dysregulated AA metabolism, excessive prostaglandin E2 (PGE2) production, aggravated inflammation, oxidative stress, and fibrosis. Conversely, adeno-associated virus (AAV)-mediated restoration of FGF21 normalized COX-derived AA metabolites, suppressed COX-2 activation, and ameliorated hepatic injury. Pharmacological inhibition of COX-2 partially recapitulated the protective effects of FGF21 but failed to reverse fibrosis, suggesting that COX-2 contributes to disease progression but is not sufficient to account for fibrosis. Mechanistically, FGF21 suppressed COX-2 through a PPARα-dependent pathway, whereas ERK1/2 phosphorylation acted upstream of the FGF21/PPARα axis. In patients with MASLD, circulating PGE2 was positively associated with liver injury after adjustment for body mass index and hepatic steatosis. Collectively, the FGF21-PPARα-COX-2 axis represents a critical regulator of AA metabolic remodeling and a potential therapeutic target for MASLD.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70999","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962570","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}

引用次数: 0

Cooccurrence of Homologous Recombination Deficiency and Mismatch Repair Deficiency in Colorectal Cancer 结直肠癌中同源重组缺陷和错配修复缺陷的共同发生

IF 14.1

MedComm Pub Date : 2026-09-15 DOI: 10.1002/mco2.70991

Xu Zhang, Hao Xu, Kailai Wang, Wangxiong Hu

{"title":"Cooccurrence of Homologous Recombination Deficiency and Mismatch Repair Deficiency in Colorectal Cancer","authors":"Xu Zhang, Hao Xu, Kailai Wang, Wangxiong Hu","doi":"10.1002/mco2.70991","DOIUrl":"https://doi.org/10.1002/mco2.70991","url":null,"abstract":"Homologous recombination deficiency (HRD) in colorectal cancer (CRC) remains largely unexplored. In contrast, mismatch repair deficiency (dMMR) occurs in ∼15% of patients with CRC. Although HRD and dMMR have historically been regarded as mutually exclusive, emerging evidence suggests that this mutual exclusivity may not be absolute. Here, we conducted a retrospective cohort study utilizing genomic and transcriptomic data to define HRD status in a Chinese dMMR CRC cohort (n = 99). Multiple machine learning approaches were employed to analyze the expression profiles of these tumors and to develop a classifier distinguishing HRD from homologous recombination proficiency (HRP) in dMMR CRCs. In the Chinese dMMR CRC cohort, 66% of tumors were classified as HRD. Compared with the HRP group, the HRD group had a significantly higher tumor mutational burden and better outcomes. The derived expression signature, comprising eight genes, successfully predicted HRD status in dMMR tumors with high accuracy in the training set (AUC = 0.88, Naïve Bayes) and the test set (AUC = 0.87). In this study, a subset of dMMR CRC tumors with co-occurring HRD was identified, which may have potential implications for patient stratification and the application of targeted therapies, such as PARP inhibitors, in this molecular subgroup.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70991","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962568","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}

引用次数: 0

Neutrophil Extracellular Traps in Atherosclerosis and Cardiovascular Disease 动脉粥样硬化和心血管疾病中的中性粒细胞胞外陷阱

IF 14.1

MedComm Pub Date : 2026-09-15 DOI: 10.1002/mco2.70912

Ji Zhang, Fangjiaqi Wei, Mengdi Qu, Yuwen Shao, Tingye Xu, Darko Stojkov, Hans-Uwe Simon, Ben Huang, Changhong Miao, Hao Zhang

{"title":"Neutrophil Extracellular Traps in Atherosclerosis and Cardiovascular Disease","authors":"Ji Zhang, Fangjiaqi Wei, Mengdi Qu, Yuwen Shao, Tingye Xu, Darko Stojkov, Hans-Uwe Simon, Ben Huang, Changhong Miao, Hao Zhang","doi":"10.1002/mco2.70912","DOIUrl":"https://doi.org/10.1002/mco2.70912","url":null,"abstract":"Atherosclerosis is a chronic inflammatory disease of the arterial wall and the leading pathological basis of cardiovascular morbidity and mortality worldwide. Neutrophil extracellular traps (NETs), web-like chromatin structures armed with histones, myeloperoxidase, and serine proteases, have emerged as active participants in vascular inflammation and thrombosis. Under physiological conditions, NETs contribute to host defense and immunothrombosis, but excessive or persistent NET formation drives endothelial injury, plaque progression, and acute coronary events. However, how NETs shift from protective to pathological across the atherosclerotic continuum, and how their individual components cooperate to amplify vascular damage, remain insufficiently understood. This review explores NET homeostasis in the cardiovascular system and the balance between protective and pathological NET release. We then describe the molecular mechanisms of NET formation and the cooperative actions of NET components as an integrated thrombo-inflammatory platform. Next, we discuss stage-specific NET roles throughout atherogenesis, plaque destabilization, and ischemia–reperfusion injury. Finally, we evaluate clinical and translational evidence linking NET biomarkers to cardiovascular outcomes and critically assess precision-targeted NET therapies. This framework highlights NETs as both mechanistic drivers and promising therapeutic targets in atherosclerotic cardiovascular disease.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70912","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962571","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}

引用次数: 0

Mucosal-Associated Invariant T Cells in Health and Disease 健康和疾病中粘膜相关的不变性T细胞

IF 14.1

MedComm Pub Date : 2026-09-15 DOI: 10.1002/mco2.70996

Yu Zhao, Feng-Mi Ou, Dan Liang, Yang Gao, Qing-Qing Li, Yi-Qun Kuang

{"title":"Mucosal-Associated Invariant T Cells in Health and Disease","authors":"Yu Zhao, Feng-Mi Ou, Dan Liang, Yang Gao, Qing-Qing Li, Yi-Qun Kuang","doi":"10.1002/mco2.70996","DOIUrl":"https://doi.org/10.1002/mco2.70996","url":null,"abstract":"Mucosal-associated invariant T (MAIT) cells are a population of evolutionarily conserved, unconventional innate-like T lymphocytes that are restricted by major histocompatibility complex Class I-related (MR1) molecules. They can be activated either in a T-cell receptor–MR1- or cytokine-dependent manner. Activated MAIT cells play crucial roles in maintaining homeostasis and the fine regulation of the immune system. This review presents a systematic exploration of the development, biological characteristics, and multiple effects of MAIT cells in health and various diseases. In healthy individuals, MAIT cells maintain mucosal barrier integrity, participate in tissue repair after injury, and prevent excessive inflammation. In microbial infections, MAIT cells eliminate infected cells and modulate immune responses or become pathogenic when overactivated by superantigens. In the context of immune-related diseases, MAIT cells migrate to inflamed tissues and become pathogenic by secreting tissue-damaging cytokines or protective by modulating immune responses. Moreover, MAIT cells have been demonstrated to have therapeutic applications in controlling diseases through their use as cellular adjuvants, their increased activation by engineered bacteria, and their modification with chimeric antigen receptors. This review synthesizes the functional plasticity of MAIT cells in health and disease, highlighting the therapeutic efficacy and limitations of engineered MAIT cells for precise intervention.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70996","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962572","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}

引用次数: 0

Post-Tuberculosis Lung Disease: Clinicopathologic Insights, Diagnosis, Prevention, and Management 结核后肺病：临床病理见解、诊断、预防和管理

IF 14.1

MedComm Pub Date : 2026-09-15 DOI: 10.1002/mco2.70974

Radha Gopalaswamy, Selvakumar Subbian

{"title":"Post-Tuberculosis Lung Disease: Clinicopathologic Insights, Diagnosis, Prevention, and Management","authors":"Radha Gopalaswamy, Selvakumar Subbian","doi":"10.1002/mco2.70974","DOIUrl":"https://doi.org/10.1002/mco2.70974","url":null,"abstract":"Post-tuberculosis lung disease (PTLD) encompasses a spectrum of chronic pulmonary abnormalities arising from tuberculosis (TB)-associated tissue injury and maladaptive repair, and is emerging as a major contributor to long-term respiratory disability among TB survivors. In this review, we position PTLD within the broader continuum of TB pathobiology, from initial host–pathogen interactions to chronic structural and functional lung sequelae. We examine current definitions, epidemiology, and clinical burden, and present mechanistic insights into the inflammatory, proteolytic, fibrotic, immunometabolic, and vascular pathways that drive persistent lung damage. We further discuss the heterogeneous clinical phenotypes of PTLD, including airflow obstruction, bronchiectasis, restrictive lung disease, pleural complications, chronic pulmonary aspergillosis, and nontuberculous mycobacterial disease, highlighting practical approaches to diagnosis, risk stratification, and management across diverse healthcare settings. We discuss PTLD in children and adolescents, prevention opportunities throughout the TB care cascade, and health-system strategies for integrating post-TB care. Finally, we identify key knowledge gaps in PTLD nosology, biomarkers, therapeutic development, clinical trial design, and implementation science. Recognition of PTLD as a continuation rather than an endpoint of TB is essential for advancing survivorship-focused care and reducing the global burden of chronic respiratory disease after TB.","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"7 10","pages":""},"PeriodicalIF":14.1,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70974","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148962569","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}

引用次数: 0

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