Journal of Cardiovascular Translational Research最新文献_第4页

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-01 Epub Date: 2025-01-09 DOI: 10.1007/s12265-024-10583-x

Xing-Jie Wang, Lei Huang, Min Hou, Jie Guo

引用次数: 0

Associations of Blood Lipid-Related Polygenic Scores, Lifestyle Factors and Their Combined Effects with Risk of Coronary Artery Disease in the UK Biobank Cohort. 英国生物库队列中血脂相关多基因评分、生活方式因素及其综合效应与冠状动脉疾病风险的关系。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-01 Epub Date: 2024-12-16 DOI: 10.1007/s12265-024-10578-8

Jungyoon Choi, Wanqing Wen, Guochong Jia, Ran Tao, Jirong Long, Xiao-Ou Shu, Wei Zheng

引用次数: 0

Prediction of Major Adverse Limb Events in Females with Peripheral Artery Disease using Blood-Based Biomarkers and Clinical Features. 利用基于血液的生物标志物和临床特征预测女性外周动脉疾病的主要肢体不良事件

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-01 Epub Date: 2024-12-06 DOI: 10.1007/s12265-024-10574-y

Ben Li, Hamzah Khan, Farah Shaikh, Abdelrahman Zamzam, Rawand Abdin, Mohammad Qadura

{"title":"Prediction of Major Adverse Limb Events in Females with Peripheral Artery Disease using Blood-Based Biomarkers and Clinical Features.","authors":"Ben Li, Hamzah Khan, Farah Shaikh, Abdelrahman Zamzam, Rawand Abdin, Mohammad Qadura","doi":"10.1007/s12265-024-10574-y","DOIUrl":"10.1007/s12265-024-10574-y","url":null,"abstract":"The objective of this study was to identify a female-specific prognostic biomarker for peripheral artery disease (PAD) and develop a prediction model for 2-year major adverse limb events (MALE). Patients with/without PAD were recruited (n=461). Plasma concentrations of 68 circulating proteins were measured and patients were followed for 2 years. The primary outcome was MALE (composite of vascular intervention, major amputation, or acute/chronic limb threatening ischemia). We trained a random forest model using: 1) clinical characteristics, 2) female-specific PAD biomarker, and 3) clinical characteristics and female-specific PAD biomarker. Galectin-9 was the only protein to be significantly elevated in females compared to males in the discovery/validation analyses. The random forest model achieved the following AUROC's: 0.72 (clinical features), 0.83 (Galectin-9), and 0.86 (clinical features + Galectin-9). We identified Galectin-9 as a female-specific PAD biomarker and developed an accurate prognostic model for 2-year MALE using a combination of clinical features and plasma Galectin-9 levels.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":"316-330"},"PeriodicalIF":2.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791801","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

Targeting Lactic Acid Modification in Ischemic Heart Diseases: Novel Therapeutics and Mechanism. 靶向乳酸修饰治疗缺血性心脏病：新疗法及机制

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-01 Epub Date: 2025-02-07 DOI: 10.1007/s12265-025-10593-3

Tangjiang Wan, Yucheng Liang, Tianwen Wei, Zijie Chen, Yafei Li

引用次数: 0

The link between ferroptosis and autophagy in myocardial ischemia/reperfusion injury: new directions for therapy. 心肌缺血/再灌注损伤中铁下垂与自噬的关系：新的治疗方向。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-01 Epub Date: 2025-01-30 DOI: 10.1007/s12265-025-10590-6

Xiaoting Yang, Hui Wu, Di Liu, Gang Zhou, Dong Zhang, Qingzhuo Yang, Yanfang Liu, Yi Li

引用次数: 0

The Role of Mitophagy in Cardiac Metabolic Remodeling of Heart Failure: Insights of Molecular Mechanisms and Therapeutic Prospects. 线粒体自噬在心力衰竭的心脏代谢重塑中的作用：分子机制和治疗前景的见解。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-03-26 DOI: 10.1007/s12265-025-10606-1

Fangying Yan, Liwen Bao

{"title":"The Role of Mitophagy in Cardiac Metabolic Remodeling of Heart Failure: Insights of Molecular Mechanisms and Therapeutic Prospects.","authors":"Fangying Yan, Liwen Bao","doi":"10.1007/s12265-025-10606-1","DOIUrl":"https://doi.org/10.1007/s12265-025-10606-1","url":null,"abstract":"Heart failure (HF) treatment remains one of the major challenges in cardiovascular disease management, and its pathogenesis requires further exploration. Cardiac metabolic remodeling is of great significance as a key pathological process in the progression of HF. The complex alterations of metabolic substrates and associated enzymes in mitochondria create a vicious cycle in HF. These changes lead to increased reactive oxygen species, altered mitochondrial Ca2+ handling, and the accumulation of fatty acids, contributing to impaired mitochondrial function. In this context, mitophagy plays a significant role in clearing damaged mitochondria, thereby maintaining mitochondrial function and preserving cardiac function by modulating metabolic remodeling in HF. This article aims to explore the role of mitophagy in cardiac metabolic remodeling in HF, especially in obesity cardiomyopathy, diabetic cardiomyopathy, and excessive afterload-induced heart failure, thoroughly analyze its molecular mechanisms, and review the therapeutic strategies and prospects based on the regulation of mitophagy.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143719377","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

Induced Human-like Coronary Stenosis in Hypercholesterolemic PCSK9 Minipigs. 高胆固醇血症PCSK9迷你猪诱导的类人冠状动脉狭窄。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-03-25 DOI: 10.1007/s12265-025-10607-0

Jacob Nicolaisen, Christian Frøsig Bo Poulsen, Martin Mæng Bjørklund, Martin Nors Skov, Maiken Kudahl Larsen, Troels Thim, Jouke Dijkstra, Jacob Fog Bentzon, Evald Høj Christiansen, Niels Ramsing Holm

{"title":"Induced Human-like Coronary Stenosis in Hypercholesterolemic PCSK9 Minipigs.","authors":"Jacob Nicolaisen, Christian Frøsig Bo Poulsen, Martin Mæng Bjørklund, Martin Nors Skov, Maiken Kudahl Larsen, Troels Thim, Jouke Dijkstra, Jacob Fog Bentzon, Evald Høj Christiansen, Niels Ramsing Holm","doi":"10.1007/s12265-025-10607-0","DOIUrl":"https://doi.org/10.1007/s12265-025-10607-0","url":null,"abstract":"Translational models for obstructive coronary artery disease are lacking. We aimed to develop a porcine model for obstructive coronary stenosis induced by bioresorbable stent (BRS) implantation in hypercholesterolemic proprotein convertase subtilisin/kexin-9 (PCSK9) minipigs. Fifteen hypercholesterolemic PCSK9 minipigs were randomized to percutaneous coronary intervention with Magmaris, Absorb or Desolve BRS. Optical coherence tomography (OCT) scans were performed at baseline and 6-months followed by histology. Matched OCT analysis showed minimal lumen area decreased from 7.62 ± 1.54 mm2 at baseline to 2.12 ± 0.92 mm2 at follow-up in the Magmaris group, from 6.99 ± 1.49 mm2 to 3.07 ± 1.52 mm2 in the Absorb group, and from 6.05 ± 1.11 mm2 to 2.65 ± 0.93 mm2 in the Desolve group. Histologic examination revealed advanced human-like stenosis. BRS implantation in hypercholesterolemic PCSK9 minipigs induced human-like stenoses and may serve as a feasible preclinical model for obstructive coronary artery disease.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709945","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

Roles of Lipoxygenases in Cardiovascular Diseases. 脂氧合酶在心血管疾病中的作用

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-03-25 DOI: 10.1007/s12265-025-10605-2

Ting Liu, Ding Ai

引用次数: 0

Inhibition of Egr2 Protects against TAC-induced Heart Failure in Mice by Suppressing Inflammation and Apoptosis Via Targeting Acot1 in Cardiomyocytes. 抑制Egr2通过靶向心肌细胞Acot1抑制炎症和凋亡来保护tac诱导的小鼠心力衰竭

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-03-17 DOI: 10.1007/s12265-025-10602-5

Xiaolu Hou, Guoling Hu, Heling Wang, Ying Yang, Qi Sun, Xiuping Bai

{"title":"Inhibition of Egr2 Protects against TAC-induced Heart Failure in Mice by Suppressing Inflammation and Apoptosis Via Targeting Acot1 in Cardiomyocytes.","authors":"Xiaolu Hou, Guoling Hu, Heling Wang, Ying Yang, Qi Sun, Xiuping Bai","doi":"10.1007/s12265-025-10602-5","DOIUrl":"https://doi.org/10.1007/s12265-025-10602-5","url":null,"abstract":"Heart failure (HF) is a clinical syndrome caused by structural or functional abnormalities in heart. Egr2 has been reported to be protective for multiple diseases, but its effect on HF remains unknown. The present study intended to investigate the potential role of Egr2 in HF and its possible downstream effectors. High Egr2 expression in heart was observed in HF mice. Egr2 knockdown alleviated cardiac damage and function in HF mice. Egr2 knockdown inhibited myocardial inflammation and apoptosis both in vivo and in vitro. Egr2 inhibited Acot1 transcription expression via directly binding to its promoter. Acot1 overexpression reduced Lipopolysaccharide (LPS)-induced cardiomyocyte inflammation and apoptosis. Functional rescue experiments revealed that Acot1 reversed the effects of Egr2 on LPS-induced cell apoptosis and inflammation. Overall, Egr2 knockdown might ameliorate HF by inhibiting inflammation and apoptosis in cardiomyocytes by targeting Acot1. This study might provide evidence to better understand the molecular mechanisms of HF pathogenesis.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648584","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

PLK1 Downregulation Attenuates ET-1-Induced Cardiomyocyte Hypertrophy by Suppressing the ERK1/2 Pathway. 下调 PLK1 可通过抑制 ERK1/2 通路减轻 ET-1 诱导的心肌细胞肥大

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-03-17 DOI: 10.1007/s12265-025-10604-3

Jie Ding, Anqi Yang, Liping Zhou, Fulei Zhang, Huixing Zhou, Yuemei Zhang, Yan Wang, Yi Liu, Dandan Liang, Yuanyuan Liu, Yahan Wu

{"title":"PLK1 Downregulation Attenuates ET-1-Induced Cardiomyocyte Hypertrophy by Suppressing the ERK1/2 Pathway.","authors":"Jie Ding, Anqi Yang, Liping Zhou, Fulei Zhang, Huixing Zhou, Yuemei Zhang, Yan Wang, Yi Liu, Dandan Liang, Yuanyuan Liu, Yahan Wu","doi":"10.1007/s12265-025-10604-3","DOIUrl":"https://doi.org/10.1007/s12265-025-10604-3","url":null,"abstract":"Cardiomyocyte hypertrophy is a key remodeling response to cardiac stress and an independent risk factor for heart failure. However, the molecular mechanism of cardiomyocyte hypertrophy is not yet fully understood. We here found Polo-like kinase 1 (PLK1) was crucial in regulating endothelin-1 (ET-1)-induced cardiomyocyte hypertrophy. Notably, PLK1 expression was significantly elevated in ET-1-induced hypertrophic cardiomyocytes and pressure overload-induced hypertrophic cardiac tissue. Knocking down Plk1 reduced the cell size of hypertrophic cardiomyocytes and suppressed the expression of hypertrophic markers, including ANP, BNP and β-MHC. The PLK1 inhibitor BI2536 had similar effects on hypertrophic cardiomyocytes. Mechanistically, the ERK1/2 pathway was identified as the key downstream pathway mediating the effects of PLK1 on ET-1-induced cardiomyocyte hypertrophy. Finally, the deficiency of PLK1 attenuated the hypertrophy of hiPSC-CMs. In summary, our study revealed that PLK1 regulates ET-1-induced cardiomyocyte hypertrophy through the ERK1/2 pathway, providing insights into the pathogenesis and potential therapies for pathological cardiac hypertrophy.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648585","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