Journal of Cardiovascular Translational Research最新文献

Fibro-Inflammatory Signaling, Fibrosis, and Microvascular Ischemia as Convergent Translational Substrates of Sudden Cardiac Death in Hypertrophic Cardiomyopathy: A Systematic Review. 纤维炎症信号、纤维化和微血管缺血作为肥厚性心肌病心源性猝死的聚合翻译底物：系统综述

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-10-13 DOI: 10.1007/s12265-026-10853-w

Antonio da Silva Menezes Junior, Isabela Jube Wastowski, Lilian Carla Carneiro

{"title":"Fibro-Inflammatory Signaling, Fibrosis, and Microvascular Ischemia as Convergent Translational Substrates of Sudden Cardiac Death in Hypertrophic Cardiomyopathy: A Systematic Review.","authors":"Antonio da Silva Menezes Junior, Isabela Jube Wastowski, Lilian Carla Carneiro","doi":"10.1007/s12265-026-10853-w","DOIUrl":"10.1007/s12265-026-10853-w","url":null,"abstract":"Hypertrophic cardiomyopathy (HCM) remains an important cause of sudden cardiac death (SCD), but the biological determinants of ventricular arrhythmic vulnerability remain incompletely defined. This systematic translational review examined whether fibro-inflammatory signaling, fibrotic remodeling, and microvascular ischemia represent convergent components of the arrhythmogenic substrate in HCM. MEDLINE/PubMed, Embase, Web of Science Core Collection, and Cochrane Library were searched from inception to January 2026. Of 167 records, 37 full-text reports were assessed and 11 studies included. Fibrosis emerged as the most clinically mature substrate marker, while microvascular ischemia appeared to amplify electrical instability, particularly in remodeled myocardium. Molecular and tissue studies suggested upstream fibro-inflammatory programs involving activated fibroblasts, extracellular matrix dysregulation, SMAD/TGF-beta signaling, CRLF1/LIFR-JAK-STAT signaling, and altered multicellular communication. Overall, the evidence supports an integrated mechanism-to-substrate model, but prospective outcome-validated studies are needed before these biological layers can refine SCD risk stratification beyond established clinical and imaging markers in contemporary HCM practice.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13661659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149182028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Higher Myocardial miR-1-3p, miR-30a-5p, miR-34a-5p, and Lower miR208a-3p Levels are Associated with Lower Age at the Time of Heart Transplantation. 较高的心肌miR-1-3p、miR-30a-5p、miR-34a-5p和较低的miR208a-3p水平与心脏移植时较低的年龄相关。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-10-08 DOI: 10.1007/s12265-026-10854-9

Vid Mirosevic, Tanja Blagus, Tomo Svagusa, Ana Livun, Petra Bakovic, Ana Sepac, Ana Kulic, Vita Dolzan, Filip Sedlic

{"title":"Higher Myocardial miR-1-3p, miR-30a-5p, miR-34a-5p, and Lower miR208a-3p Levels are Associated with Lower Age at the Time of Heart Transplantation.","authors":"Vid Mirosevic, Tanja Blagus, Tomo Svagusa, Ana Livun, Petra Bakovic, Ana Sepac, Ana Kulic, Vita Dolzan, Filip Sedlic","doi":"10.1007/s12265-026-10854-9","DOIUrl":"10.1007/s12265-026-10854-9","url":null,"abstract":"Expression of microRNAs (miR-1-3p, miR-21-3p, miR-30a-5p, miR-34a-5p, miR-133a-3p, miR-208a-3p, and miR-423-5p) and mitochondrial unfolded protein response (UPRmt) genes (HSPA9, HSPD1, LONP1, OMA1, and YME1L) was investigated by qRT-PCR in six controls and 65 failing human hearts (33 ischemic cardiomyopathy (ICM), 28 dilated cardiomyopathy (DCM), 2 hypertrophic cardiomyopathy, and 1 non-compaction and restrictive cardiomyopathy each). Failing hearts had higher expression of miR-208a-3p, HSPA9, HSPD1, OMA1, YME1L and lower miR-1-3p expression compared to controls. Patients with higher miR-1-3p, miR-30a-5p, miR-34a-5p, (miR-423-5p exhibited a trend) and lower miR-208a-3p expression underwent heart transplantation or LVAD implantation earlier in life. DCM group had higher expression of miR-1-3p, miR-30a-5p, HSPD1, and LONP1 compared to the ICM group. Thus, myocardial expression of miR-1-3p, miR-30a-5p, miR-34a-5p, and miR-208a-3p could be associated with the HF progression; miR-208a-3p, HSPA9, HSPD1, OMA1, YME1L, and miR-1-3p could discriminate HF form control; and miR-1-3p, miR-30a-5p, HSPD1, and LONP1 could discriminate DCM from ICM.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

α7-nAChR Activation is Associated with Attenuation of Cardiac Fibrosis in Ischemic Cardiomyopathy via SIRT3-Dependent Modulation of EndMT. α7-nAChR激活与缺血性心肌病心肌纤维化衰减相关，通过sirt3依赖性调节EndMT。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-10-08 DOI: 10.1007/s12265-026-10857-6

Ruilin He, Shujie Wu, Que Xu, Yifan Lin, Xiaohui Niu, Suwei Weng, Jiafeng Lin

引用次数: 0

YAP and WWTR1/TAZ Connect Mechanotransduction and Mitochondrial Metabolism in Cardiac Hypertrophy and Ventricular Remodeling. YAP和WWTR1/TAZ在心肌肥厚和心室重构中的机械转导和线粒体代谢之间的联系

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-10-08 DOI: 10.1007/s12265-026-10858-5

Feihu Yu, Zuqiu Liu, Jimiao Qiu, Huashan Chen, Xiaowei Song, Songqun Huang, Changjin Li

{"title":"YAP and WWTR1/TAZ Connect Mechanotransduction and Mitochondrial Metabolism in Cardiac Hypertrophy and Ventricular Remodeling.","authors":"Feihu Yu, Zuqiu Liu, Jimiao Qiu, Huashan Chen, Xiaowei Song, Songqun Huang, Changjin Li","doi":"10.1007/s12265-026-10858-5","DOIUrl":"10.1007/s12265-026-10858-5","url":null,"abstract":"Cardiac hypertrophy is a mechanometabolic remodeling process shaped by mechanical load, matrix stiffness and mitochondrial adaptation. YAP and TAZ, encoded by YAP1 and WWTR1, are paralogous, non-DNA-binding transcriptional co-activators that link cytoskeletal tension to TEAD-dependent transcription. This review organizes current evidence along a mechanical stress-YAP/TAZ activation-mitochondrial remodeling-ventricular remodeling axis and distinguishes direct human myocardial data, animal cardiac mechanisms, related cardiovascular or in vitro evidence, and cross-disease extrapolation. Experimental studies suggest that TEAD1 supports mitochondrial gene programs, transient YAP activation promotes glycolytic compensation during early pressure overload, whereas sustained Yap1 activation may impair mitochondrial biogenesis. Cell-specific studies further implicate fibroblast, endothelial, immune and epicardial programs, although many data derive from non-hypertrophic contexts. Thus, the adaptive-to-maladaptive YAP/TAZ model remains provisional. Human lineage-resolved data are limited, and no YAP/TAZ-targeted therapy is established for cardiac hypertrophy.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Stacking Ensemble Learning for Diagnosing Acute Myocardial Infarction in Mice Using Plasma Raman Spectroscopy and Mass Spectrometry. 利用等离子体拉曼光谱和质谱技术对小鼠急性心肌梗死进行堆叠集成学习诊断。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-10-07 DOI: 10.1007/s12265-026-10856-7

Chunyan Duan, Jing Sun, Shijun Chen, Zhengshi Wang, Lin Sun, Chengyou Jia, Xiankai Li

{"title":"Stacking Ensemble Learning for Diagnosing Acute Myocardial Infarction in Mice Using Plasma Raman Spectroscopy and Mass Spectrometry.","authors":"Chunyan Duan, Jing Sun, Shijun Chen, Zhengshi Wang, Lin Sun, Chengyou Jia, Xiankai Li","doi":"10.1007/s12265-026-10856-7","DOIUrl":"10.1007/s12265-026-10856-7","url":null,"abstract":"Cardiac troponin is the reference biomarker for acute myocardial infarction (AMI) but has limited utility in the hyperacute phase. Raman spectroscopy enables rapid, label-free molecular analysis, whereas mass spectrometry offers greater molecular specificity at higher cost. Plasma from 57 coronary-ligated or Sham-operated mice underwent Raman spectroscopy and mass spectrometry. A stacking ensemble model was developed to identify AMI using Raman spectroscopy, mass spectrometry, or fused data. Under nested cross-validation, the Raman spectroscopy model yielded an area under the receiver operating characteristic curve (AUC) of 0.807 (95% CI [0.679, 0.910]). Mass spectrometry and fused models achieved 1.000 (95% CI [1.000, 1.000]), and fusion showed no detectable improvement over mass spectrometry. Cardiac troponin I demonstrated 0.714 (95% CI [0.567, 0.842]), significantly lower than mass spectrometry and fused models (Holm-adjusted p < 0.001) and numerically lower than the Raman spectroscopy model (Holm-adjusted p = 0.357). These findings require confirmation in larger human cohorts.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149127604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Deep Survival Modeling With Echocardiographic Myocardial Texture Radiomics for Prediction of Major Adverse Cardiovascular Events in Hypertrophic Cardiomyopathy. 超声心动图心肌结构放射组学深度生存模型预测肥厚性心肌病主要不良心血管事件。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-10-02 DOI: 10.1007/s12265-026-10845-w

Guizi Liang, Jiangyu Han, Xiaolan Huang, Xing Chen, Dongwei Xie, Limei Liang, Rentao Zhi, Shengjiang Chen, Bulin Zhang, Yan Deng

{"title":"Deep Survival Modeling With Echocardiographic Myocardial Texture Radiomics for Prediction of Major Adverse Cardiovascular Events in Hypertrophic Cardiomyopathy.","authors":"Guizi Liang, Jiangyu Han, Xiaolan Huang, Xing Chen, Dongwei Xie, Limei Liang, Rentao Zhi, Shengjiang Chen, Bulin Zhang, Yan Deng","doi":"10.1007/s12265-026-10845-w","DOIUrl":"10.1007/s12265-026-10845-w","url":null,"abstract":"Hypertrophic cardiomyopathy (HCM) carries substantial risk of major adverse cardiovascular events (MACE), yet current tools do not fully exploit quantitative myocardial texture from routine echocardiography. We retrospectively studied 413 patients with HCM from two tertiary centers to develop and externally validate a deep survival model integrating transthoracic echocardiographic texture radiomics with clinical and conventional echocardiographic variables. Patients from one center (n = 308) were used for development and internal testing and those from the other (n = 105) for external validation. The best-performing model was selected by cross-validated Harrell C-index and interpreted using Shapley additive explanations. During median follow-up of 30.7 and 35.6 months, 83 patients (20.1%) experienced a first MACE. The Combined model showed the highest concordance and net clinical benefit, with age, RadScore, left atrial diameter, and maximal wall thickness as leading contributors. This model may provide an accessible approach to individualised MACE risk stratification in HCM.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Diagnostic Accuracy of Circulating MicroRNAs for Coronary Artery Disease: An Updated Systematic Review and Meta-analysis. 循环microrna对冠状动脉疾病的诊断准确性：最新的系统综述和荟萃分析。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-10-01 DOI: 10.1007/s12265-026-10848-7

Shankar Biswas, Yashasvi Srivastava, Ayman Hamadttu

{"title":"Diagnostic Accuracy of Circulating MicroRNAs for Coronary Artery Disease: An Updated Systematic Review and Meta-analysis.","authors":"Shankar Biswas, Yashasvi Srivastava, Ayman Hamadttu","doi":"10.1007/s12265-026-10848-7","DOIUrl":"10.1007/s12265-026-10848-7","url":null,"abstract":"Circulating microRNAs (miRNAs) are promising non-invasive biomarkers for coronary artery disease (CAD). We conducted an updated meta-analysis evaluating their diagnostic accuracy through December 2025. PubMed, Embase, and Scopus were searched for diagnostic accuracy studies of circulating miRNAs in angiography-confirmed CAD. Accuracy was pooled using a bivariate random-effects model yielding sensitivity, specificity, and SROC-AUC. Twenty-four studies (64 comparisons, 3,879 participants) were included. Pooled sensitivity was 0.777 (95% CI: 0.737-0.816), specificity 0.832 (95% CI: 0.801-0.862), and AUC 0.872. Multi-miRNA panels outperformed single miRNAs (AUC 0.901 vs. 0.868). Substantial heterogeneity was present (Sensitivity; I²=92.1%; τ²=0.738); however, τ² remained substantial (sens:0.738, tfpr:0.434), indicating persistent heterogeneity; Holling-adjusted I² (5.1-7.7%) reflects sensitivity to study precision, not resolved heterogeneity. Meta-regression identified panel-based assay type and plasma sample source as modifiable drivers. Circulating miRNAs show moderate-to-good diagnostic accuracy for CAD as investigational complementary biomarkers. Prospective validation with standardized protocols is required before clinical deployment. PROSPERO Registration ID: CRD420261279673. Not Applicable (As this is a Systematic Review and Meta-analysis and not a Clinical Trial).","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction Note: lncRNA HOTAIR Protects Myocardial Infarction Rat by Sponging miR-519d-3p. 备注：lncRNA HOTAIR通过海绵化miR-519d-3p保护心肌梗死大鼠。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-10-01 DOI: 10.1007/s12265-026-10850-z

Dongying Zhang, Bingjian Wang, Min Ma, Kun Yu, Qing Zhang, Xiwen Zhang

引用次数: 0

Metabolite-based Analysis of High-Risk Factors on Occurrence of AKI in Patients with Acute Myocardial Infarction. 基于代谢物的急性心肌梗死患者AKI高危因素分析

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-09-29 DOI: 10.1007/s12265-026-10849-6

Yan Yao, Fei Liu, Jie Meng, JinJing Zhang, MingXing Chen, Tianqing Cao

引用次数: 0

Suppression of Calpain Attenuates Coxsackievirus B3-Induced Myocarditis by Regulating RIPK1/RIPK3/MLKL Pathway. 抑制Calpain通过调控RIPK1/RIPK3/MLKL通路减轻柯萨奇病毒b3诱导的心肌炎

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-09-28 DOI: 10.1007/s12265-026-10744-0

Yuxi Liu, Yong Wang, Guijian Liu, Fei Yi, Dongyang Che, Zhiwei Chen, Yunzeng Zou, Ruizhen Chen

{"title":"Suppression of Calpain Attenuates Coxsackievirus B3-Induced Myocarditis by Regulating RIPK1/RIPK3/MLKL Pathway.","authors":"Yuxi Liu, Yong Wang, Guijian Liu, Fei Yi, Dongyang Che, Zhiwei Chen, Yunzeng Zou, Ruizhen Chen","doi":"10.1007/s12265-026-10744-0","DOIUrl":"10.1007/s12265-026-10744-0","url":null,"abstract":"Viral myocarditis caused by CVB3 inflicts substantial myocardial damage and predisposes to heart failure. Although necroptosis contributes to disease progression, the mechanisms governing this death pathway during CVB3 infection remain unclear. We found that calpain and its inhibitor Cast were dynamically expressed during CVB3 infection, correlating with cardiac damage, inflammation, and fibrosis. Further investigation revealed that CVB3 dynamically induced cardiomyocyte necroptosis by activating the RIPK1/RIPK3/MLKL pathway, which was prominently activated in the early acute phase but potentially attenuated in later stages. Immunofluorescence analysis supported the translocation of p-MLKL from the nucleus to the plasma membrane during disease progression. Importantly, both in vivo and in vitro experiments supported that calpain inhibition ALLN attenuated VMC via the RIPK1/RIPK3/MLKL pathway, and improved cardiac function post-CVB3 infection. The calpain activator PMMA exacerbated this process. Our findings reveal that calpain inhibition attenuated VMC by modulating the RIPK1/RIPK3/MLKL pathway, uncovering a novel regulatory mechanism in VMC.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13619709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0