Experimental Biology and Medicine最新文献

{"title":"Transcriptomics-based identification of shared biomarkers across type 2 diabetes, mild cognitive impairment, and uric acid metabolism.","authors":"Yan Liu, Dongmei Kang, Yuan Lei","doi":"10.3389/ebm.2026.11060","DOIUrl":"10.3389/ebm.2026.11060","url":null,"abstract":"<p><p>Uric acid metabolism is associated with the development of type 2 diabetes mellitus (T2DM), cardiometabolic, and cardiovascular diseases. Additionally, T2DM patients often exhibit mild cognitive impairment (MCI). However, the underlying mechanisms remain unclear. This study aims to identify and validate biomarkers associated with uric acid metabolism in T2DM and MCI, with the goal of discovering potential diagnostic and therapeutic targets to improve the quality of life for T2DM patients. Transcriptomic data for T2DM, MCI and uric acid metabolism-related genes were sourced from public databases. Biomarkers were screened using machine learning and validated for expression. Subsequent analyses included functional enrichment, immune infiltration, subcellular localization, and drug prediction. Three biomarkers-HP, ITGB3, and SELP-were identified. All showed significantly elevated expression in the T2DM group (p < 0.05). HP and ITGB3 were primarily enriched in ribosome-related pathways, primary immunodeficiency, and adherens junction processes. Immune infiltration analysis revealed that immature B cells and plasmacytoid dendritic cells were significantly enriched in T2DM. HP showed the strongest positive correlation with plasmacytoid dendritic cells (cor = 0.65, FDR <0.05), while ITGB3 exhibited the strongest positive correlation with immature B cells (cor = 0.76, FDR <0.05). Several potential therapeutic drugs were predicted, including calcifediol (score = -99.93) and meclofenamic acid (score = -99.89). This study identified three candidate biomarkers co-dysregulated across T2DM and MCI transcriptomes and associated with uric acid metabolism. Given the exploratory sample sizes, these findings are considered hypothesis-generating and require validation in larger independent cohorts.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11060"},"PeriodicalIF":3.8,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13381339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148600856","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":"Mitochondrial transfer and mesenchymal stem cells in ophthalmology: current evidence and therapeutic implications.","authors":"Xiaoli Liu, Mingqi Zhang, Zhuoshi Wang","doi":"10.3389/ebm.2026.11128","DOIUrl":"10.3389/ebm.2026.11128","url":null,"abstract":"<p><p>Mitochondrial dysfunction, driven by genetic mutations or oxidative stress, is a central contributor to the onset and progression of ophthalmic diseases. In recent years, intercellular mitochondrial transfer (MT) has emerged as a novel mechanism of cellular communication and repair in ocular tissues. MT occurs through tunneling nanotubes, extracellular vesicles (EVs), cell fusion, or transmitophagy, and has been shown to support photoreceptor survival, maintain retinal homeostasis, and protect against oxidative injury. Mesenchymal stem cells (MSCs), owing to their remarkable reparative and immunomodulatory properties, have attracted particular attention as efficient mitochondrial donors. Evidence from experimental models demonstrates that MSC-mediated MT can restore bioenergetics, mitigate oxidative stress, and rescue cellular function in inherited optic neuropathies, corneal injuries, retinal degenerative diseases, and ischemic retinopathies. This review summarizes current evidence of MT in ophthalmology, highlights the therapeutic contributions of MSCs, discusses the molecular and microenvironmental factors regulating MT efficiency, and outlines unresolved challenges. We further provide perspectives on how mitochondrial transfer may be translated into innovative therapies for ocular disorders.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11128"},"PeriodicalIF":3.8,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13364729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445303","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":"Advances in research on pharmacological mechanisms of anatabine: from nicotinic modulation to multitarget therapeutic potential.","authors":"Xiaonan Li, Xiaomin Liu, Huaquan Sheng, Jianfeng Guo, Leihao Zhang, Ting Fei, Yihan Gao","doi":"10.3389/ebm.2026.11069","DOIUrl":"10.3389/ebm.2026.11069","url":null,"abstract":"<p><p>Anatabine, a characteristic minor alkaloid derived from tobacco byproducts, exhibits unique structural analogy to nicotine but possesses a superior safety profile and lower addictive liability, rendering it a promising natural multi-target therapeutic candidate. Accumulating preclinical evidence has demonstrated that anatabine exerts neuroprotective, anti-inflammatory, and antioxidant effects mainly through modulating α7/α4β2 nicotinic acetylcholine receptors, suppressing NF-κB/STAT3 inflammatory signaling, and activating the Nrf2-mediated antioxidant pathway. It effectively ameliorates typical pathological alterations, including β-amyloid deposition, tau hyperphosphorylation, and microglial overactivation, thereby improving cognitive and behavioral deficits in neurodegenerative disease models. Additionally, anatabine displays broad pharmacological potentials in chronic inflammation, autoimmune thyroiditis, asthma, and hypertension. Differing from previous reviews that merely focused on single receptor regulation, the present work systematically summarizes the multi-target pharmacological characteristics of anatabine, comprehensively collates its preclinical efficacy across multiple disease categories, and highlights its advantages over nicotine in safety and addiction risk. Furthermore, we analyze the current limitations, druggability optimization challenges, and clinical translation prospects, and propose sustainable strategies for high-value utilization of tobacco byproducts. This review provides an updated and systematic theoretical basis for further mechanism exploration and therapeutic development of anatabine.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11069"},"PeriodicalIF":3.8,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13357314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148435655","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":"Phenotypic profiling of Pathogen Box compounds MMV667494 and MMV028694 in bloodstream-form <i>Trypanosoma brucei brucei</i>.","authors":"Pearl Ihuoma Akazue, Neils Ben Quashie, Sue Vaughan, Harry P de Koning, Theresa Manful Gwira","doi":"10.3389/ebm.2026.10979","DOIUrl":"10.3389/ebm.2026.10979","url":null,"abstract":"<p><p>Open-access drug discovery platforms have accelerated hit identification and lead prioritization across multiple diseases and enable systematic repurposing of bioactive compounds beyond their original indications. However, there remains a need for new chemotypes for African trypanosomiasis with improved efficacy and resilience to emerging drug resistance. In this study, we evaluated the antitrypanosomal potential and cellular effects of two Pathogen Box compounds, MMV667494 and MMV028694. The compounds were selected through a resazurin-based <i>in vitro</i> phenotypic viability screen that measures metabolic activity as a proxy for parasite viability against bloodstream-form <i>Trypanosoma brucei brucei</i>. To explore cellular phenotypes consistent with potential mechanisms of action, we applied cytological profiling using flow cytometry- and microscopy-based assays, including Annexin V/propidium iodide staining, cell-cycle DNA-content analysis, mitochondrial membrane potential (TMRE), and mitochondrial reactive oxygen species (MitoSOX) measurements. Both MMV667494 and MMV028694 (IC₅₀ = 0.44 ± 0.05 µM and 0.33 ± 0.03 µM, respectively) displayed sub-micromolar antitrypanosomal potency and preferential toxicity toward trypanosomes over mammalian cells (selectivity indices >10). Growth profiling demonstrated dose-dependent inhibition of parasite proliferation, with evidence of trypanocidal activity at higher concentrations and longer exposure times. Treatment resulted in increased populations of phosphatidylserine-exposed and membrane-compromised cells, which is consistent with apoptosis-like phenotypes in trypanosomes. Although both compounds induced mitochondrial membrane depolarization in treated <i>T. b. brucei</i> cells, this effect was observed predominantly in a subpopulation of cells and is therefore unlikely to represent the primary cause of cell death. Increased mitochondrial production of reactive oxygen species and altered cell-cycle progression were also observed, which might indicate disruption of key cellular processes. These findings shows that MMV667494 and MMV028694 are selective antitrypanosomal compounds and their activities are associated with induce apoptosis-like features, cell-cycle disruption, and mitochondrial stress signatures in bloodstream-form <i>T. b. brucei</i>. These findings provide phenotypic insights into the activity of the compounds, warranting further target deconvolution and optimization, although validation in human-infective subspecies and <i>in vivo</i> systems will be required.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10979"},"PeriodicalIF":3.8,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13303395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148344335","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":"Nicotinamide adenine dinucleotide phosphate oxidase 4 in lung disease: a review of its biology and therapeutic potential.","authors":"Yilin Wang, Tianru Ben, Jianjiang Fang, Zengpan Li, Jinhua Ding, Liyan Xu, Kai Lin, Li Jiang","doi":"10.3389/ebm.2026.10941","DOIUrl":"10.3389/ebm.2026.10941","url":null,"abstract":"<p><p>Nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) is a constitutively active enzyme that primarily produces hydrogen peroxide, a reactive oxygen species (ROS) with diverse cellular functions. While initially recognized for its role in oxidative stress, emerging evidence suggests that NOX4 plays a pivotal role in the pathogenesis of various lung diseases. This review delineates the structure characteristics of NOX4, emphasizing how its domain organization underlies a distinctive mode of molecular regulation. It further discusses current knowledge on the biological functions of NOX4-derived oxygen species, including their roles in modulating inflammation, cell death pathways, oxygen sensing, nuclear signaling, and metabolic reprogramming. Through these interconnected processes, NOX4 is positioned as a central mediator linking redox imbalance to cellular dysfunction. In addition, the contribution of NOX4 to the pathogenesis of major lung diseases, including idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), asthma, acute lung injury/acute respiratory distress syndrome (ALI/ARDS), and pulmonary hypertension are critically evaluated. Emerging therapeutic strategies targeting NOX4 are also discussed, together with key challenges associated with clinical translation, including isoform specificity, off-target effects, and tissue-selective delivery. Overall, this review provides an integrated framework for understanding NOX4 biology across multiple levels and highlights its potential as a therapeutic target in lung disease.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10941"},"PeriodicalIF":3.8,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13303397/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148344339","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":"High systolic blood pressure and stroke: evidence from the NHANES 1999-2023 and global burden of disease 2021.","authors":"LuYi Tang, BoWen Yang, PeiWen Li, YingQi Chen, Yi Liu, Ting Wang, Xiaohan Ye","doi":"10.3389/ebm.2026.10868","DOIUrl":"10.3389/ebm.2026.10868","url":null,"abstract":"<p><p>High systolic blood pressure (HSBP) is a major modifiable risk factor for stroke, but trends in disease burden and causal associations related to HSBP in the United States require further investigation using multidimensional approaches. This study aims to elucidate this relationship by utilizing data from the Global Burden of Disease (GBD) database, the National Health and Nutrition Examination Survey (NHANES). This study integrated data from the GBD 2021 database and the NHANES. The GBD data provided macro-level estimates of stroke-related mortality and disability-adjusted life years (DALYs) attributable to various risk factors within the United States. By employing multivariable logistic regression models on individual-level NHANES data, the study assessed the association between HSBP history and stroke risk after adjusting for multiple confounding factors. GBD analysis revealed HSBP as the leading risk factor for U.S. stroke burden in 2021, with an increasing attributable burden since 2010, particularly among the elderly and women. NHANES analysis showed that HSBP significantly increased the risk of stroke (fully adjusted OR = 1.33, 95% CI: 1.17-1.51). Elevated SBP was additionally associated with increased all-cause mortality risk in stroke survivors (HR = 1.01). A novel U-shaped relationship emerged: stroke risk decreased below an SBP of 100 mmHg but increased sharply above this threshold. HSBP is the core driver and modifiable risk factor behind the persistently increasing stroke burden in the United States. The findings of this study highlight the critical importance of HSBP in stroke prevention and management.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10868"},"PeriodicalIF":3.8,"publicationDate":"2026-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13283930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148307867","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":"Scaling human liver microphysiological systems: implementing a higher-throughput liver acinus microphysiological system platform.","authors":"Dillon C Gavlock, Michael W Castiglione, Allen Wang, Mahboubeh Varmazyad, Lawrence A Vernetti, Mark E Schurdak, D Lansing Taylor, Jacquelyn A Brown, Mark T Miedel","doi":"10.3389/ebm.2026.11038","DOIUrl":"10.3389/ebm.2026.11038","url":null,"abstract":"<p><p>The advancement in the use of all-human high content microphysiological systems (MPS) has enabled better <i>in vitro</i> modeling of liver function and disease progression as well as drug efficacy, metabolism and toxicity (ADME-Tox) testing. However, a continuing need in liver MPS development is balancing throughput without loss of the high-content biological complexity required for physiologically relevant modeling. Here, we present a scalable version of our well-established liver acinus microphysiological system (LAMPS). This higher-throughput format (ht-LAMPS) is designed to recapitulate the physiological complexity of the standard single-chamber LAMPS system while increasing experimental capacity through a seven-chamber microfluidic design. The ht-LAMPS is constructed using the same four key liver cell types as the LAMPS: primary hepatocytes and liver sinusoidal endothelial cells (LSECs) as well as Kupffer-like cells (THP-1) and hepatic stellate cells (LX-2). It recapitulates key physiological characteristics previously established in the LAMPS platform, including oxygen zonation-dependent liver phenotypes including model viability, secretion of functional and cytotoxicity markers, mitochondrial activity, and lipid accumulation, demonstrating reproducibility in the ht-LAMPS format. Finally, we also demonstrate that the ht-LAMPS model recapitulates key phenotypes associated with the progression of metabolic dysfunction-associated steatotic liver disease (MASLD), including increased steatosis and elevated production of inflammatory cytokines and profibrotic markers using our established MASLD media formulations. Overall, by increasing throughput while maintaining key high-content biological features of the LAMPS, ht-LAMPS provides a scalable platform for investigating liver function, modeling disease progression, and enabling downstream drug testing in MASLD and other liver-related conditions.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11038"},"PeriodicalIF":3.8,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13236629/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148197806","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":"Race, oxygen exposure, and retinopathy of prematurity: re-examining a persistent epidemiologic paradox.","authors":"Beryl Zhou, Sarah H Rodriguez, Alexis Warren, Dimitra Skondra","doi":"10.3389/ebm.2026.11094","DOIUrl":"10.3389/ebm.2026.11094","url":null,"abstract":"<p><p>Retinopathy of prematurity (ROP) is a leading cause of childhood blindness that arises from disrupted retinal vascular development in premature infants. Oxygen exposure remains a central driver of treatment-warranted ROP, as higher saturation levels suppress early retinal vascular growth and later promote pathological neovascularization. Large, randomized trials of oxygen targeting show that lower oxygen saturation ranges reduce the incidence of treatment-requiring ROP, though with trade-offs in mortality. Observational cohorts, including the CRYO-ROP, ETROP, and e-ROP trials, consistently report lower rates of treatment-warranted ROP and reduced treatment need among Black infants despite similar or greater prematurity risk. Multiple explanations have been proposed to account for the paradoxically lower rates of treatment-warranted ROP observed among Black infants. Although biologic variations in angiogenic pathways have been proposed, evidence suggests that structural and clinical factors may offer an alternative explanation for these patterns. Black race is strongly correlated with residence in neighborhoods with greater socioeconomic disadvantage, which is associated with increased risk of prematurity and missed ROP follow-up visits. In addition, pulse oximeters may overestimate oxygen saturation in individuals with darker skin pigmentation, potentially altering targeted oxygen exposure. Survival-related selection bias may further contribute to this paradox, as infants at the highest risk of both mortality and treatment-warranted ROP may not survive long enough to develop treatment-requiring disease. This review examines racial differences in ROP severity and examines how oxygen exposure and structural factors may contribute to these disparities, while acknowledging the limited evidence supporting biologic explanations.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"11094"},"PeriodicalIF":3.8,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13222856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148149012","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":"Peripheral immune cells and glycation indices as potential diagnostic biomarkers in amyotrophic lateral sclerosis.","authors":"Xue Yang, Jing Yang, Rui Li, Hui Dong, Yaling Liu","doi":"10.3389/ebm.2026.10987","DOIUrl":"10.3389/ebm.2026.10987","url":null,"abstract":"<p><p>The diagnosis of amyotrophic lateral sclerosis (ALS) mainly relies on clinical symptoms and the exclusion of other diseases, with a lack of specific biomarkers, leading to delayed diagnosis and a high rate of misdiagnosis. This study aims to explore the utility of peripheral immune cells and glycosylation indices as potential diagnostic biomarkers for ALS to enhance the accuracy and efficiency of early ALS diagnosis. This retrospective study included 54 ALS patients diagnosed in our hospital from June 2023 to October 2024, along with 54 healthy controls. Blood samples and laboratory data, including levels of peripheral immune cells and glycosylation indices, were collected from both groups. Through logistic regression, random forest models, receiver operating characteristic (ROC) curve analysis, and SHAP interpretability analysis, the predictive abilities and clinical significance of each candidate indicator were screened and evaluated. Notable disparities were detected in age, leukocyte count, monocyte levels, glycated haemoglobin A1c (HbA1c), and haemoglobin glycation index (HGI) between the control and ALS groups (all <i>P</i> < 0.05). Logistic regression analysis revealed that age (OR = 1.114) and monocyte (OR = 3.174) were risk factors for ALS, while leukocyte (OR = 0.533) and HbA1c (OR = 0.069) were protective factors. The random forest algorithm, ranked by decreasing importance, showed that leukocyte, HGI, monocyte, and HbA1c level all influenced ALS. Using these indicators to predict ALS resulted in a false-positive rate of 18% and a false-negative rate of 6%. ROC curve analysis indicated that the combined use of leukocyte, monocyte, HbA1c level, and HGI provided the highest diagnostic value for ALS (AUC = 0.774), which was higher than that of any individual indicator (all <i>P</i> < 0.05). SHAP analysis visualization demonstrated that increased monocyte and decreased leukocyte, HGI, and HbA1c level were all associated with an increased risk of ALS onset, ranked in descending order of feature importance as monocyte, leukocyte, HGI, and HbA1c. Peripheral blood white blood cells, monocytes, HbA1c, and HGI can serve as potential diagnostic biomarkers for ALS. Combined detection can improve the diagnostic accuracy of ALS, facilitating early diagnosis and intervention, and ultimately improving patient prognosis. Further validation in cohorts including disease controls is required to confirm specificity.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10987"},"PeriodicalIF":3.8,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13212250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053680","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":"Antibody-mediated immune responses and cardiovascular disease: a Mendelian randomization study.","authors":"Yi Li, Jiuqi Fan, Lirong Wu","doi":"10.3389/ebm.2026.10945","DOIUrl":"10.3389/ebm.2026.10945","url":null,"abstract":"<p><p>Cardiovascular diseases represent the leading cause of global mortality and disability, posing a severe threat to human health. Accumulating evidence suggests that antigen-antibody-mediated immune responses may be involved in the pathogenesis of various cardiovascular conditions; however, whether these associations reflect causal relationships has long remained unclear. To address this question, we conducted a bidirectional two-sample Mendelian randomization study leveraging summary-level data from genome-wide association studies. In this analysis, 46 antibody-mediated immune traits were evaluated as exposures, and 11 cardiovascular outcomes, including aortic aneurysm, aortic valve stenosis, atrial fibrillation, coronary artery disease, dilated cardiomyopathy, atrioventricular block, heart failure with reduced ejection fraction, hypertrophic cardiomyopathy, infective endocarditis, myocarditis, and pericarditis, were examined as outcomes. Our results revealed several significant causal associations: genetically predicted higher levels of Epstein-Barr virus EBNA-1 antibodies were associated with increased risks of myocarditis and aortic valve stenosis, while elevated VCA p18 antibody levels were linked to a higher risk of myocarditis. Furthermore, increased antibody levels against BK polyomavirus VP1 were causally associated with greater risks of aortic valve stenosis and dilated cardiomyopathy. In contrast, higher levels of antibodies against varicella-zoster virus glycoproteins and human herpesvirus 6 IE1B were associated with reduced risks of myocarditis and aortic aneurysm, respectively. These findings not only help clarify the causal role of immune-mediated mechanisms in cardiovascular pathogenesis but also provide a theoretical foundation for the future development of immune-targeted strategies for prevention and treatment.</p>","PeriodicalId":12163,"journal":{"name":"Experimental Biology and Medicine","volume":"251 ","pages":"10945"},"PeriodicalIF":3.8,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13201210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148041523","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}