Journal of Cardiovascular Translational Research最新文献_第6页

RE1-Silencing Transcription Factor: an Atheroprotective Regulator in the Vascular Endothelium. re1沉默转录因子：血管内皮中的动脉粥样硬化保护调节因子。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-07-06 DOI: 10.1007/s12265-026-10795-3

Luzhang Ji, Xinpeng Li, Shuqin Liu, Yihua Bei

引用次数: 0

Correction: A Hidden Indicator of Cardiovascular Health: Serum Gamma-Glutamyl Transferase in Focus. 修正：心血管健康的一个隐藏指标：血清γ -谷氨酰转移酶的焦点。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-07-03 DOI: 10.1007/s12265-026-10813-4

Akanksha Saini, Manik, Zaid Bashir, Dinesh Kumar Mehta, Savita Kumari, Rina Das

引用次数: 0

ChemoCardioNet: An Explainable Multimodal Transformer for Early Prediction of Chemotherapy-Induced Cardiotoxicity. chemcardionet：一个可解释的多模态变压器，用于化疗引起的心脏毒性的早期预测。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-07-02 DOI: 10.1007/s12265-026-10807-2

Sarada Prasad Dakua

{"title":"ChemoCardioNet: An Explainable Multimodal Transformer for Early Prediction of Chemotherapy-Induced Cardiotoxicity.","authors":"Sarada Prasad Dakua","doi":"10.1007/s12265-026-10807-2","DOIUrl":"10.1007/s12265-026-10807-2","url":null,"abstract":"Chemotherapy-induced cardiotoxicity (CIC) remains a major cause of morbidity and mortality among cancer survivors, and conventional monitoring often fails to detect early subclinical cardiac injury. We propose ChemoCardioNet, an explainable multimodal deep learning framework that predicts cardiotoxicity risk before clinical manifestation by integrating electrocardiograms (ECG), echocardiography, clinical variables, and serum biomarkers. The architecture combines modality-specific encoders, including 1D convolutional transformers for ECG sequences, CNN-ViT hybrid blocks for echocardiographic frames, and multilayer perceptrons for clinical and biomarker features. A cross-attention fusion transformer aligns latent representations across modalities and captures temporal evolution across chemotherapy cycles. The model outputs a probabilistic cardiotoxicity risk score with feature-level explainability using SHAP analysis. In a cohort of 1,200 patients, ChemoCardioNet achieved an AUC of 0.92, outperforming single-modality and traditional machine learning approaches by 8-12%. The model predicted cardiotoxicity approximately two cycles before detectable echocardiographic dysfunction, supporting earlier risk identification and improved cardio-oncology monitoring.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13328215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148368585","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

Metabolic Heterogeneity Across Heart Failure Subtypes Defined by Integrative Multi-Omics Analysis. 通过综合多组学分析确定心力衰竭亚型的代谢异质性。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-06-30 DOI: 10.1007/s12265-026-10803-6

Yuzhou Xue, Lin Liu, Ming Xu, Ling Jin

{"title":"Metabolic Heterogeneity Across Heart Failure Subtypes Defined by Integrative Multi-Omics Analysis.","authors":"Yuzhou Xue, Lin Liu, Ming Xu, Ling Jin","doi":"10.1007/s12265-026-10803-6","DOIUrl":"10.1007/s12265-026-10803-6","url":null,"abstract":"Heart failure (HF) is a heterogeneous syndrome with diverse etiologies, yet the metabolic determinants specific to its subtype remain unclear. We performed an integrative multi-omics analysis combining metabolomics, genetics, and single-cell transcriptomics to characterize metabolic signatures of distinct HF subtypes. By applying Mendelian randomization of 1,091 circulating metabolites, we identified distinct metabolic patterns: lipid metabolites, particularly sphingolipids, were associated with increased HF risk, while tricarboxylic acid (TCA) cycle intermediates exhibited potential protective effects. Subtype-specific differences included lipid remodeling in coronary heart disease (CHD)-related HF, TCA metabolism in hypertension (HTN)-related HF, and amino acid pathways in overweight-related HF. Integrative analyses highlighted candidate regulators such as UPP1, NEU3, CBS, SHMT1, PLD2, OGDHL, and SULT1A1/2. Single-cell data revealed cardiomyocyte-enriched expression of OGDHL, which was consistently downregulated in experimental HF models. These findings provide insight into metabolic heterogeneity in HF and identify OGDHL as a potential regulator of cardiac metabolic remodeling.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148360860","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

The Immediate Impact of Infarct Size on the Systemic Inflammatory Response: IL-6 as Central Mediator Identified through Biomarker and Proteomic Profiling. 梗死面积对全身炎症反应的直接影响：通过生物标志物和蛋白质组学分析鉴定出IL-6作为中心介质。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-06-29 DOI: 10.1007/s12265-026-10801-8

Jonathan Los, Frans B Mensink, Özlem Bulut, Ilse H Hol, Aysun Cetinyurek-Yavuz, Niels P Riksen, Saloua El Messaoudi, Jan H Cornel, Robert-Jan M van Geuns

{"title":"The Immediate Impact of Infarct Size on the Systemic Inflammatory Response: IL-6 as Central Mediator Identified through Biomarker and Proteomic Profiling.","authors":"Jonathan Los, Frans B Mensink, Özlem Bulut, Ilse H Hol, Aysun Cetinyurek-Yavuz, Niels P Riksen, Saloua El Messaoudi, Jan H Cornel, Robert-Jan M van Geuns","doi":"10.1007/s12265-026-10801-8","DOIUrl":"10.1007/s12265-026-10801-8","url":null,"abstract":"Myocardial infarction (MI) induces an inflammatory response that may be amenable to targeted therapy. This cohort study evaluated the systemic inflammatory burden across different infarct sizes using serial measurements of C-reactive protein (CRP), interleukin-6 (IL-6), and targeted inflammatory proteomics (Olink's Target 96 Inflammation panel) during hospitalization and up to 12 weeks post-MI. Baseline IL-6 concentrations were progressively higher with increasing infarct size, with differential temporal trajectories observed across infarct size strata (P for interaction < 0.001), a finding confirmed by proteomic analysis (Padj for interaction = 0.009). Patients with small infarct size showed no significant changes in CRP or IL-6 concentrations, yet demonstrated downregulation of urokinase (uPA) and upregulation of angiogenesis-related proteins (tumor necrosis factor-related weak inducer of apoptosis [TWEAK] and hepatocyte growth factor [HGF]), similar to those observed in patients with moderate or large infarct sizes, emphasizing the biological significance of these processes. Overall, greater myocardial injury was associated with higher inflammatory burden, highlighting IL-6 as a promising therapeutic target for acute anti-inflammatory treatment after large MI.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13314833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148351994","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

Tracing the pathogenic PLN p.(Arg14del) variant across the globe; more than just a local curiosity. 在全球范围内追踪致病性PLN p.（Arg14del）变异；不仅仅是当地的奇珍异宝。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-06-25 DOI: 10.1007/s12265-026-10792-6

Esmée van Drie, Freyja H M van Lint, Rob Zwart, Jie Wang, Yucheng Chen, Alex V Postma, Martin G Elferink, Joris J M van Steenbrugge, Paul A van der Zwaag, Jan D H Jongbloed, Dennis Dooijes, Myrthe Y C van der Heide, Arjan C Houweling, Kristina H Haugaa, Ida Skrinde Leren, Anna Kostareva, Hendrik Milting, Thuy Vy Nguyen, Thuy Duong Ho Huynh, Philippe Chevalier, Antoine Delinière, Juan R Gimeno-Blanes, María Sabater-Molina, Roberto Barriales-Villa, Andrea Mazzanti, Mirella Memmi, Yuki Kuramoto, Tomoka Tabata, Arthur A M Wilde, Karin Y van Spaendonck-Zwarts, J Peter van Tintelen

{"title":"Tracing the pathogenic PLN p.(Arg14del) variant across the globe; more than just a local curiosity.","authors":"Esmée van Drie, Freyja H M van Lint, Rob Zwart, Jie Wang, Yucheng Chen, Alex V Postma, Martin G Elferink, Joris J M van Steenbrugge, Paul A van der Zwaag, Jan D H Jongbloed, Dennis Dooijes, Myrthe Y C van der Heide, Arjan C Houweling, Kristina H Haugaa, Ida Skrinde Leren, Anna Kostareva, Hendrik Milting, Thuy Vy Nguyen, Thuy Duong Ho Huynh, Philippe Chevalier, Antoine Delinière, Juan R Gimeno-Blanes, María Sabater-Molina, Roberto Barriales-Villa, Andrea Mazzanti, Mirella Memmi, Yuki Kuramoto, Tomoka Tabata, Arthur A M Wilde, Karin Y van Spaendonck-Zwarts, J Peter van Tintelen","doi":"10.1007/s12265-026-10792-6","DOIUrl":"10.1007/s12265-026-10792-6","url":null,"abstract":"Studying the global distribution of the pathogenic variant c.40_42delAGA;p.(Arg14del) in the phospholamban (PLN) gene is highly important for raising awareness among healthcare providers and may help uncover factors contributing to variability in the development of associated cardiomyopathy phenotypes. PLN p.(Arg14del)-positive individuals were identified through a PubMed literature search, our clinical and research networks, and ClinVar. Additionally, population prevalences were determined using publicly available genetic databases. Furthermore, haplotype analysis was conducted using haplotype markers or whole genome sequencing data to assess whether newly identified cases across different continents share common ancestry. The PLN p.(Arg14del) variant was identified in 21 countries across four continents. Haplotype marker analysis suggest that most analyzed individuals, except those from Greece, shared at least part of a common haplotype. The PLN p.(Arg14del) variant is present in at least 2000 carriers globally. While the majority share at least part of a common haplotype, suggesting a common founder, data suggest an independent mutational event in Greek patients.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13303328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148329690","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

Extracellular Vesicles Link Cerebral Ischemia to Coronary Microvascular Dysfunction - Role for RGD Motif-Activated Endothelin Signaling. 细胞外小泡将脑缺血与冠状动脉微血管功能障碍联系起来——RGD基序激活的内皮素信号的作用。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-06-25 DOI: 10.1007/s12265-026-10802-7

Marta Balogh, Melina Tangos, Vijay S Patel, Nazha Hamdani, Zsolt Bagi

{"title":"Extracellular Vesicles Link Cerebral Ischemia to Coronary Microvascular Dysfunction - Role for RGD Motif-Activated Endothelin Signaling.","authors":"Marta Balogh, Melina Tangos, Vijay S Patel, Nazha Hamdani, Zsolt Bagi","doi":"10.1007/s12265-026-10802-7","DOIUrl":"10.1007/s12265-026-10802-7","url":null,"abstract":"Ischemic stroke is associated with increased risk of subsequent cardiac ischemic events, yet mechanisms linking cerebral ischemia to coronary dysfunction remain unclear. We hypothesized that ischemic stroke directly impairs coronary microvascular function through circulating factors released after cerebral ischemia. We found that the vasodilator function of coronary arterioles (CA) was reduced in patients with prior ischemic stroke. In rats, transient middle cerebral artery occlusion impaired CA vasodilator function. Extracellular vesicles (EVs) isolated after cerebral ischemia and delivered into the rat CA lumen also impaired vasodilation. Moreover, we found that luminal delivery of RGD peptide attenuated flow-induced vasodilation in rat CA, an effect that was prevented by BQ-123, an endothelin ETA receptor antagonist. We propose that ischemic stroke directly induces coronary microvascular dysfunction via circulating EV-mediated, RGD-motif-dependent activation of endothelin signaling. This brain-heart vascular axis provides a mechanistic basis for increased post-stroke coronary risk and identifies EV-mediated pathways as potential therapeutic targets.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148329697","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

Immunometabolic Remodeling in Ischemic and Non-Ischemic Heart Failure. 缺血性和非缺血性心力衰竭的免疫代谢重塑。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-06-24 DOI: 10.1007/s12265-026-10800-9

Xiaoyun Zang, Guangdong Zhang, Silin Kong, Chao Zhao, Xiaodong Sun, Kexin Zhang

{"title":"Immunometabolic Remodeling in Ischemic and Non-Ischemic Heart Failure.","authors":"Xiaoyun Zang, Guangdong Zhang, Silin Kong, Chao Zhao, Xiaodong Sun, Kexin Zhang","doi":"10.1007/s12265-026-10800-9","DOIUrl":"10.1007/s12265-026-10800-9","url":null,"abstract":"Heart failure (HF) is traditionally classified by etiology or ejection fraction, but these categories do not fully explain the mechanisms driving disease progression. Increasing evidence suggests that both ischemic and non-ischemic HF are shaped by maladaptive interactions between immune activation and metabolic remodeling. In ischemic HF, acute cardiomyocyte death and reperfusion stress trigger a phase dependent inflammatory response requiring coordinated adaptation across immune, vascular, stromal, and myocardial cells. In non-ischemic HF, chronic cardiometabolic and hemodynamic stress impairs metabolic fitness in these compartments, promoting endothelial dysfunction, mitochondrial injury, fibrosis, and loss of myocardial reserve. Despite distinct triggers, both phenotypes converge on a shared immunometabolic substrate marked by inflammatory persistence, impaired metabolic flexibility, organelle stress, redox imbalance, and fibroinflammatory remodeling. This review highlights failed immunometabolic state transitions as a unifying mechanism in HF and examines roles for immune and metabolic memory, organelle stress networks, mitochondrial lipid crosstalk, and regulated lipid peroxidation.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148308263","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

Left Ventricular Thrombus in Ischemic Heart Failure: Machine-learning-based Prediction of Six-month Persistence and One-year Outcomes. 缺血性心力衰竭左心室血栓：基于机器学习的6个月持续性和1年预后预测。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-06-22 DOI: 10.1007/s12265-026-10804-5

Yunus Emre Yavuz, Yakup Alsancak, Sefa Tatar, Hayri İncekara, Büşra Özyeşi̇l, Hakan Akilli, Abdullah İçli̇

{"title":"Left Ventricular Thrombus in Ischemic Heart Failure: Machine-learning-based Prediction of Six-month Persistence and One-year Outcomes.","authors":"Yunus Emre Yavuz, Yakup Alsancak, Sefa Tatar, Hayri İncekara, Büşra Özyeşi̇l, Hakan Akilli, Abdullah İçli̇","doi":"10.1007/s12265-026-10804-5","DOIUrl":"10.1007/s12265-026-10804-5","url":null,"abstract":"Left ventricular thrombus (LVT) in ischemic heart failure carries embolic risk; tools to anticipate persistence are limited. We studied 190 consecutive patients with imaging-confirmed LVT managed with guideline-concordant anticoagulation and serial echocardiography. The primary outcome was 6-month non-regression; 1-year MACE was secondary. We combined classical statistics with explainable machine learning. CatBoost yielded the best discrimination for non-regression (CV-AUC 0.76; test accuracy 0.79). SHAP highlighted left atrial diameter, pulmonary artery pressure, platelet count, and LV end-diastolic diameter as leading predictors. For 1-year outcomes, thrombus size and CHA2DS2-VA were independently associated with MACE (logistic AUC 0.71), whereas \"regression vs persistence\" alone was not. Baseline remodeling and coagulability markers, captured by an interpretable ML model, stratify early risk of LVT persistence and complement clinical decision-making for imaging follow-up and anticoagulation intensity.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13287210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295120","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

Pim1 Mitigates Heart Failure by Suppressing Ferroptosis Via Activation of the mTORC1/SLC7A11/GPX4 Axis. Pim1通过激活mTORC1/SLC7A11/GPX4轴抑制铁下沉减轻心力衰竭。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-06-19 DOI: 10.1007/s12265-026-10805-4

Yunrui Zhang, Fanqi Kong, Weiwei Wang, Jiaxi Pan

{"title":"Pim1 Mitigates Heart Failure by Suppressing Ferroptosis Via Activation of the mTORC1/SLC7A11/GPX4 Axis.","authors":"Yunrui Zhang, Fanqi Kong, Weiwei Wang, Jiaxi Pan","doi":"10.1007/s12265-026-10805-4","DOIUrl":"10.1007/s12265-026-10805-4","url":null,"abstract":"Heart failure (HF) remains a major cause of morbidity and mortality, with ferroptosis increasingly implicated in its progression. Pim1, a serine/threonine kinase, exerts cardioprotective effects by regulating cell survival and oxidative stress, but its role in ferroptosis during HF remains unclear. Here, HF was induced in rats by left anterior descending coronary artery ligation, followed by lentiviral-mediated Pim1 overexpression. Cardiac function, myocardial injury, fibrosis, and ferroptosis-related markers were evaluated. In vitro, H9C2 cardiomyocytes were exposed to H2O2 or Erastin to model HF-related injury and ferroptosis. Pim1 overexpression significantly improved cardiac function, alleviated myocardial injury and fibrosis, and suppressed ferroptosis by reducing Fe²⁺, ROS, and lipid peroxidation while enhancing GSH and GPX4 activity. Mechanistically, Pim1 regulated the mTORC1/SLC7A11/GPX4 axis, whereas rapamycin abrogated these protective effects. Furthermore, the rescue experiments indicated that ferroptosis suppression is the primary mechanism of Pim1‑mediated protection. Collectively, Pim1 mitigates HF progression by inhibiting ferroptosis through mTORC1/SLC7A11/GPX4 signaling.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148277563","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