Open Medicine最新文献

{"title":"Translating microbial knowledge into clinical biofilm therapies.","authors":"Abdulaziz Al Mouslem, Ghallab Alotaibi, Abdullah Alkhammash, Shinu Pottathil","doi":"10.1515/med-2026-1544","DOIUrl":"10.1515/med-2026-1544","url":null,"abstract":"<p><p>Biofilms are highly organized microbial communities that adhere to living or nonliving surfaces and are enclosed in a self-produced extracellular matrix. Their tolerance against antimicrobial agents and host defenses makes them a major challenge across clinical, industrial, and environmental fields. This review offers an in-depth analysis of biofilm formation, structure, and dispersal mechanisms, highlighting the genetic and molecular regulators that underlie their development. This review also provides extensive details of advanced and investigative strategies for biofilm eradication, including antibody-based approaches, photodynamic therapy, nanotechnology-driven solutions, surface modification of biomaterials, biological and phage-based approaches, the integration of smart and responsive systems, and host immune modulation methods. By integrating recent advances in imaging, experimental modeling, therapeutic innovations, artificial intelligence, and machine learning models, this work highlights not only the complexity of biofilm biology but also the research and development prospects for effective intervention tools. Finally, this review discusses major translational challenges associated with moving antibiofilm strategies from laboratory research to clinical and device-related applications. This review also proposes practical guidelines to overcome these challenges. Overall, the review highlights the requirements for interdisciplinary collaboration across microbiology, materials science, clinical medicine, and regulatory frameworks. Unlike traditional descriptive reviews, this review adopts a decision-oriented framework, providing clear research guidance for researchers.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261544"},"PeriodicalIF":1.8,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081343","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}

{"title":"Behavioral motivation support versus personalized dietary management for metabolic and behavioral outcomes in MASLD: a network meta-analysis.","authors":"Chao Wang, Ziying Huang, Pan Liu, Niuniu Sun, Lanhong Ruan, Mengyuan Qiao","doi":"10.1515/med-2026-1542","DOIUrl":"10.1515/med-2026-1542","url":null,"abstract":"<p><strong>Objectives: </strong>MASLD has a prevalence of almost one-third in adults worldwide and is not currently treated pharmacologically with a first-line therapy. Lifestyle change is still the foundation of management; however, the relative effectiveness of behavioral and dietary approaches remains uncertain. We compared behavioral motivation support (BMS), biomarker-guided personalized dietary management (BPDM), general dietary education (GDE), and prescribed dietary models (PDM) with usual care (UC) in adults with MASLD.</p><p><strong>Methods: </strong>Eight databases and two trial registers were searched from inception to 31 March 2026. The review record was first submitted to PROSPERO on 17 April 2026 and formally registered on 18 April 2026 (CRD420261371973), after the search but before data extraction. Random-effects frequentist NMA was used where networks were sufficiently connected; outcomes measured with different instruments were analyzed using Hedges' g or narratively.</p><p><strong>Results: </strong>Fourteen RCTs (n=1,805) were included. Compared with UC, BMS was associated with lower ALT (MD -7.41 U/L, 95 % CI -11.07 to -3.76) and BMI (MD -1.34 kg/m², 95 % CI -2.31 to -0.37), while BPDM was associated with lower ALT (MD -6.72 U/L, 95 % CI -11.76 to -1.68), BMI (MD -1.82 kg/m², 95 % CI -3.15 to -0.50), and body weight (MD -6.66 kg, 95 % CI -8.47 to -4.86). The HbA1c network was sparse and did not include BMS. Nutrition behavior was analyzed as an exploratory two-study pairwise meta-analysis (Hedges' g 1.64, 95 % CI -0.25 to 3.52), and self-efficacy was synthesized narratively. CINeMA confidence was very low across all 88 assessed network comparisons.</p><p><strong>Conclusions: </strong>The findings are hypothesis-generating and do not establish superiority, complementary clinical roles, or treatment recommendations. Direct comparative trials are required.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261542"},"PeriodicalIF":1.8,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621874/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081296","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}

{"title":"Exogenous H₂S suppresses traumatic stress-induced changes of HMGB1 and ERS in rat liver and lungs.","authors":"Qingjie Zhang, Jianfeng Lu, Zhenyong Gu","doi":"10.1515/med-2026-1501","DOIUrl":"10.1515/med-2026-1501","url":null,"abstract":"<p><strong>Objectives: </strong>Traumatic stress triggers systemic inflammation and organ injury via HMGB1 and endoplasmic reticulum stress (ERS), but whether H₂S modulates this pathway remains unclear. This study aimed to investigate the effects of exogenous H₂S (NaHS, an H₂S donor) on traumatic stress-induced HMGB1 and ERS changes in rat liver and lungs.</p><p><strong>Methods: </strong>Male SD rats underwent bilateral hindlimb crush. Sixty rats were assigned to sham, crush, NaHS pretreatment (14, 28, 56 μmol/kg), delayed NaHS (120 μmol/kg), and NaHS-only groups (n=6). Serum ALT/AST, histopathology, HMGB1 (ELISA/IHC), and ERS markers (GRP78, caspase-12, CHOP, IRE1α) were assessed.</p><p><strong>Results: </strong>Crush increased ALT/AST, liver/lung injury, plasma HMGB1, cytoplasmic HMGB1 translocation, and ERS activation. NaHS at 28 μmol/kg offered strongest protection, reducing all parameters. The 14 μmol/kg dose had limited effect; 56 μmol/kg showed reduced efficacy and mild toxicity. Delayed 120 μmol/kg also attenuated injury and HMGB1-ERS activation, though less effectively than 28 μmol/kg pretreatment.</p><p><strong>Conclusions: </strong>Exogenous H₂S attenuates traumatic stress-induced acute liver/lung injury, likely by inhibiting the HMGB1-mediated ERS pathway. Optimal protection occurs at 28 μmol/kg, while higher doses exhibit biphasic effects. These findings may inform forensic and critical care strategies.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261501"},"PeriodicalIF":1.8,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081315","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}

{"title":"Crossroads of well-being: oral health, neurology, neuronutrition and healthy aging.","authors":"Ksenia Popovskaya, Anastasiia Badaeva, Anastasiia Kosareva, Viacheslav Novikov, Andrey Danilov, Alexey Danilov, Vittorio Calabrese, Luay Rashan, Gaetano Isola, Alexander Sobin, Bekhruz Rasamatov, Vladimir Kotenev, Eva Gosteeva, Daria Archakova, Ekatherina Vitish, Artem Zacharyan, Margarita Sachkova, Alena Popova, Vlada Korlykhanova, Vitalina Rudenok","doi":"10.1515/med-2026-1515","DOIUrl":"10.1515/med-2026-1515","url":null,"abstract":"<p><p>Oral health is increasingly recognized as a critical component of systemic and neurological resilience during aging. In particular, the oral microbiome may represent a modifiable interface linking periodontal inflammation, neuroimmune activation, and the risk of neurodegenerative disorders.Emerging evidence increasingly supports a link between oral microbiome dysbiosis and the pathogenesis of neurodegenerative disorders. Chronic inflammatory conditions, such as periodontitis, are associated with systemic inflammation, which may contribute to neuroinflammation. Key oral pathogens can translocate into the systemic circulation, compromise the integrity of the blood-brain barrier, and activate microglia. Mechanisms linking oral microbiome dysbiosis to neurodegeneration include systemic inflammation mediated by pro-inflammatory cytokines, direct bacterial invasion of the central nervous system, and modulation of the oral-gut-brain axis through alterations in the gut microbiota and neuroimmune interactions. Personalized neuronutritional strategies, including dietary intake and supplementation with polyphenols, may improve oral health and reduce systemic inflammation. The interdisciplinary integration of neurology, dentistry, and neuronutrition offers new opportunities for the prevention and management of neurodegenerative disorders. Promising approaches include the development of early diagnostic biomarkers of oral dysbiosis and targeted interventions aimed at restoring microbial homeostasis. Further research is needed to clarify causal relationships and optimize strategies for modulating the oral microbiome to preserve cognitive function.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261515"},"PeriodicalIF":1.8,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13614830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149063317","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}

{"title":"GC-MS metabolomics reveals potential biomarkers for infection-specific subtypes in sepsis.","authors":"Cheng Chen, Xinna Zhao","doi":"10.1515/med-2026-1539","DOIUrl":"10.1515/med-2026-1539","url":null,"abstract":"<p><strong>Objectives: </strong>Sepsis remains one of the most severe complications of infection. Specific and easily measurable biomarkers could help us predict the type of infection in sepsis. This study aimed to explore biomarkers for early identification of sepsis with different infection.</p><p><strong>Methods: </strong>Serum was obtained from 37 patients with sepsis and 8 healthy individuals. Metabolites were screened using gas chromatography-mass spectrometry (GC-MS), and then potential biomarkers were screened. Receiver operating characteristic curve (ROC) analysis was used to evaluate potential biomarkers.</p><p><strong>Results: </strong>A total of 24 differential metabolites were found between sepsis subgroup with pulmonary infection and healthy controls, and they were enriched with 8 metabolic pathways. Similarly, 27 differential metabolites were identified in abdominal infection cases, and 64 in urinary tract infection (UTI) cases, which were associated with 23 and 26 metabolic pathways, respectively. Hydroxylamine and N-acetylputrescine may be used as candidate biomarkers to distinguish pulmonary infection and abdominal infection in sepsis, respectively, while glucose, phosphoenolpyruvate and d-ribose were good discriminators in UTI.</p><p><strong>Conclusions: </strong>Our GC-MS-based metabolomic study identified potential biomarkers for sepsis across various infection types. These biomarkers show promise for the rapid and precise diagnosis of sepsis onset. Our GC-MS-based metabolomic study identified candidate metabolites associated with different infection sources in sepsis. Given the limited sample size and the correspondingly limited statistical power, these findings are exploratory and require prospective validation in an adequately powered, independent cohort before any diagnostic application can be considered.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261539"},"PeriodicalIF":1.8,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149040345","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}

{"title":"Characterizing insomnia and sleep quality in a cohort with tension type headache.","authors":"Elena Korabelnikova, Vasilii Tkachenko, Alexey Danilov, Anastasiia Badaeva, Luay Rashan, Sergio Modafferi, Damiano Galimberti, Andrea Cavallaro, Ekaterina Vitish, Anastasiia Vitish, Viacheslav Novikov, Alena Sidenkova, Vittorio Calabrese","doi":"10.1515/med-2026-1500","DOIUrl":"10.1515/med-2026-1500","url":null,"abstract":"<p><strong>Objectives: </strong>Emerging literature data indicate insomnia as an risk factor for headache or migraine onset. It is generally recognized that headache and insomnia represent very common and major complaints worldwide, while finding exisit that indicate a symmetrical association, with headache being more associated with insomnia than the other way around. Therefore, in the association of headache and insomnia, other factors associated with headache or migraine probably play a role, as well. The aim of the study was to evaluate the clinical and pathogenetic relationships between insomnia and chronic tension-type headache (CTTH).</p><p><strong>Methods: </strong>A prospective cohort study included 65 patients with CTTH and comorbid chronic insomnia. Participants underwent clinical evaluation, assessment of headache severity (VAS, HIT-6), insomnia (PSQI, ISI), emotional state (Beck, Sheehan scales), and quality of life (SF-12). A subset (n=17) underwent polysomnography (PSG).</p><p><strong>Results: </strong>All patients reported poor sleep quality. A significant discrepancy was found between subjective sleep perception and objective PSG data (p<0.001). Patients with more severe insomnia had significantly higher levels of anxiety (p<0.001), depression (p=0.025), central sensitization (p<0.001), and lower quality of life (p<0.002). Correlation analysis revealed that worse sleep parameters (e.g., reduced REM, increased wakefulness) were associated with higher headache impact, emotional distress, and central sensitization, particularly in the mild insomnia group.</p><p><strong>Conclusions: </strong>Insomnia in CTTH patients exacerbates the condition not primarily by intensifying pain itself, but by amplifying its negative impact on emotional state and quality of life, and by strengthening the interconnections between various clinical and psychophysiological manifestations. Treating insomnia is crucial for improving overall patient well-being and pain tolerance.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261500"},"PeriodicalIF":1.8,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149040440","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}

{"title":"The role of vitamin D against biochemical indices and oxidative stress in the heart of rats exposed to diazinon.","authors":"Fateme Khodaverdi, Rasool Haddadi, Mehdi Ramezani, Fereshteh Mehri, Akram Ranjbar","doi":"10.1515/med-2026-1410","DOIUrl":"10.1515/med-2026-1410","url":null,"abstract":"<p><strong>Objectives: </strong>Diazinon is used as an organophosphate for pest management in agriculture and veterinary practice. However, diazinon poisoning can lead to increased production of free radicals and destruction of the body's antioxidant system. A study explored the impact of vitamin D on diazinon-induced cardiotoxicity in rats.</p><p><strong>Methods: </strong>24 male Wistar rats were randomly assigned to four groups: a control group treated with corn oil, a vitamin D group receiving 0.2 mg/kg/ip/day, and a DZN group receiving 70 mg/kg/po/day. Additionally, treatment groups were formed that received both DZN (70 mg/kg/po/day) and vitamin D (0.2 mg/kg/ip/day). On the final day of the experiment, the rats were euthanized, and their blood was analyzed for serum levels of troponin (TPI) and creatine kinase (CK). Furthermore, the heart tissue's concentrations of superoxide dismutase (SOD), catalase (CAT), total antioxidant capacity (TAC), total thiol groups (TTG), and malondialdehyde (MDA) were assessed. Hematoxylin and eosin (H&E)-stained slides were also used to analyze histopathological alterations in the cardiac tissue.</p><p><strong>Results: </strong>DZN significantly increased the levels of TPI, CK, and MDA, which may indicate cardiac damage. In addition, DZN decreased the levels of CAT, TAC, SOD, and TTG. On the contrary, vitamin D significantly reduced oxidative damage and increased antioxidant activities in animals with DZN. Also, these findings had a good correlation with histopathological changes.</p><p><strong>Conclusions: </strong>Vitamin D, as an antioxidant, enhances antioxidant activities in heart tissue; it effectively prevents oxidative damage caused by DZN.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261410"},"PeriodicalIF":1.8,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149040399","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}

{"title":"Differences in the burden and temporal trend of stroke in the Belt and Road Initiative countries, 1990-2021.","authors":"Zheng Luo, Yue Zhang, Huihui Lv, Jinyi Wu, Xiaopan Li","doi":"10.1515/med-2026-1532","DOIUrl":"10.1515/med-2026-1532","url":null,"abstract":"<p><strong>Objectives: </strong>To analyze the differences in the burden and trend of disability caused by stroke in \"Belt and Road\" (\"B&R\") countries from 1990 to 2021.</p><p><strong>Methods: </strong>We applied GBD 2021 to compare stroke incidence, mortality, the years lived with disability (YLDs) and disability-adjusted life-years (DALYs) from 1990 to 2021 in the \"B&R\" countries. The average annual percent change (AAPC) was used to analyze the temporal trends of age-standardized YLDs rate of stroke from 1990 to 2021 by Joinpoint regression analysis.</p><p><strong>Results: </strong>China, India and Indonesia had the highest absolute stroke numbers of stroke. From 1990 to 2021, the AAPC values of age-standardized metrics showed a downward trend in most of \"B&R\" countries. Turkmenistan had the highest increase in AAPCs of age-standardized YLDs rate for men (AAPC=0.60 %), while for women Philippines had the highest increase (AAPC=0.57 %). For under 15 years, YLDs due to stroke in most member states showed a downward trend, while increasing trends were noted in Saudi Arabia and Turkmenistan. Globally, metabolic, environmental/occupational and behavioral risk factors showed significant reductions (AAPC: -0.12 %, -0.92 %, and -0.53 %, respectively).</p><p><strong>Conclusions: </strong>The overall burden of stroke remains enormous, with regional, age and gender disparities. Enhanced health cooperation among B&R countries is warranted.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261532"},"PeriodicalIF":1.8,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13604947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149040363","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}

{"title":"Readmission rates among patients with cirrhosis across different follow-up periods and prevalence of major complications: a systematic review and meta-analysis.","authors":"Ruiyu Xie, Xiaotong Jing, Minghui Wang","doi":"10.1515/med-2026-1488","DOIUrl":"10.1515/med-2026-1488","url":null,"abstract":"<p><strong>Objectives: </strong>To estimate pooled readmission rates among adults with cirrhosis at 30 days, 90 days and 1 year after index hospitalization, and to describe the prevalence of major cirrhosis-related complications among 30-day readmitted patients.</p><p><strong>Methods: </strong>PubMed, Embase, Web of Science and the Cochrane Library were searched from inception to February 7, 2025 without language restrictions. Readmission was defined as rehospitalization after discharge from an index hospitalization, using the definition and ascertainment window reported by each included study. Pooled proportions were estimated using a random-effects model with Freeman-Tukey double-arcsine transformation. Heterogeneity was assessed using the Chi-square test and I² statistic. Sensitivity analyses were conducted, and small-study effects were explored using funnel plots and Egger's test when sufficient studies were available.</p><p><strong>Results: </strong>Thirteen cohort studies involving 316,705 patients with cirrhosis were included. The studies were published from 2015 to 2022 and sample sizes ranged from 111 to 134,038 patients. Nine studies reported 30-day readmission rates ranging from 15 % to 46 %, with a pooled estimate of 27 % (95 % CI: 20-35 %; I²=100.0 %, heterogeneity p<0.001). Five studies reported 90-day readmission rates ranging from 25 % to 53 %, with a pooled estimate of 34 % (95 % CI: 29-40 %; I²=99.6 %, heterogeneity p<0.001). Two studies reported 1-year readmission, with an exploratory pooled estimate of 33 % (95 % CI: 26-39 %; I²=97.7 %, heterogeneity p<0.001).</p><p><strong>Conclusions: </strong>Readmission after hospitalization for cirrhosis is common across short- and longer-term follow-up windows. However, the pooled estimates should be interpreted cautiously because heterogeneity was extreme, definitions varied across studies, and the 1-year estimate was based on only two studies. Ascites was the most frequently reported complication among 30-day readmitted patients, but the available data do not establish that ascites independently increases readmission risk.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261488"},"PeriodicalIF":1.8,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13603070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149040412","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}

{"title":"ID2 attenuates post-MI ventricular arrhythmias by targeting GATA4 suppression to preserve mitochondrial function and Na⁺/K⁺-ATPase activity.","authors":"Gang Pan, Shihao Huang, Xuewen Wang, Mingxin Liu, Yuanhua Xu","doi":"10.1515/med-2026-1518","DOIUrl":"10.1515/med-2026-1518","url":null,"abstract":"<p><strong>Objectives: </strong>Post-myocardial infarction (MI) ventricular arrhythmia (VA) remains a leading cause of sudden cardiac death. Current antiarrhythmic drugs often fail to target the core metabolic-structural remodeling underlying arrhythmias. The transcriptional repressor ID2, which has been implicated in cardiovascular development, remains poorly characterized regarding its role and contribution to VA pathogenesis. This study investigated the role of the transcriptional repressor ID2 in post-myocardial infarction ventricular arrhythmia.</p><p><strong>Methods: </strong>An MI rat model was established via left anterior descending (LAD) coronary artery ligation. ID2 expression in myocardial tissues was quantified by immunofluorescence and western blot. Flow cytometry and biochemical assays were employed to evaluate the impact of ID2 modulation on arrhythmogenesis. Hypoxia-challenged cardiomyocytes treated with rotenone (Complex I inhibitor) and digoxin (Na⁺/K⁺-ATPase inhibitor) were used to investigate ID2's effects on mitochondrial dysfunction and Na⁺/K⁺-ATPase activity. Mechanistic studies of ID2 included STRING interaction detection, immunofluorescence, and Pearson correlation analysis.</p><p><strong>Results: </strong>ID2 expression was significantly downregulated in MI rats and was inversely correlated with PVC frequency and VT/VF duration. Overexpression of ID2 reduced arrhythmia severity scores and attenuated PVC/VT/VF incidence in MI rats; me'anwhile, it ameliorated mitochondrial dysfunction, as reflected by restored membrane potential and ATP levels and reduced ROS, and improved Na⁺/K⁺-ATPase dysregulation in hypoxia-induced cardiomyocytes. Mechanistically, ID2 directly bound to GATA4 and reduced its expression. Overexpression of ID2 attenuated mitochondrial dysfunction and preserved Na⁺/K⁺-ATPase activity in hypoxic cardiomyocytes, whereas GATA4 overexpression weakened ID2's protective effect.</p><p><strong>Conclusions: </strong>This study demonstrates that ID2 alleviates VA by suppressing GATA4 expression, thereby mitigating mitochondrial dysfunction and Na⁺/K⁺-ATPase dysregulation. These findings elucidate the ID2-GATA4 regulatory axis in VA pathogenesis, which may provide a previously unrecognized therapeutic target for arrhythmia management.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"21 1","pages":"20261518"},"PeriodicalIF":1.8,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13596124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149025747","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}