Journal of Cardiovascular Translational Research最新文献

The Impact of Opioids on Epigenetic Modulation in Myocardial Ischemia and Reperfusion Injury: Focus on Non-coding RNAs. 阿片类药物对心肌缺血再灌注损伤表观遗传调控的影响：以非编码rna为重点。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-08 DOI: 10.1007/s12265-025-10609-y

Mohsen Davari, Mahmoud Khansari, Sahar Hosseini, Reza Morovatshoar, Alireza Azani, Seyedeh Tarlan Mirzohreh, Mohammadjavad Ashrafi Mahabadi, Moein Ghasemi, Mohammad Saeed Soleimani Meigoli, Sima Foroughi Nematollahi, Sina Pourranjbar, Qumars Behfar, Mandana Baghdadi, Ahmad Mir Hosseini

{"title":"The Impact of Opioids on Epigenetic Modulation in Myocardial Ischemia and Reperfusion Injury: Focus on Non-coding RNAs.","authors":"Mohsen Davari, Mahmoud Khansari, Sahar Hosseini, Reza Morovatshoar, Alireza Azani, Seyedeh Tarlan Mirzohreh, Mohammadjavad Ashrafi Mahabadi, Moein Ghasemi, Mohammad Saeed Soleimani Meigoli, Sima Foroughi Nematollahi, Sina Pourranjbar, Qumars Behfar, Mandana Baghdadi, Ahmad Mir Hosseini","doi":"10.1007/s12265-025-10609-y","DOIUrl":"https://doi.org/10.1007/s12265-025-10609-y","url":null,"abstract":"Myocardial ischemia-reperfusion injury (IRI) is a major issue in cardiovascular medicine, marked by tissue damage from the restoration of blood flow after ischemia. Opioids, known for their pain-relieving properties, have emerged as potential cardioprotective agents in IRI. Recent research suggests opioids influence epigenetic mechanisms-such as histone modifications and non-coding RNAs (ncRNAs)-which are essential for regulating gene expression and cellular responses during myocardial IRI. This review delves into how opioids like remifentanil affect histone modifications, DNA methylation, and ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Remifentanil postconditioning (RPC) reduces apoptosis in cardiomyocytes through histone deacetylation, specifically downregulating histone deacetylase 3 (HDAC3). Similarly, opioids impact miRNAs such as miR- 206 - 3p and miR- 320 - 3p, and lncRNAs like TINCR and UCA1, which influence apoptosis, inflammation, and oxidative stress. Understanding these interactions highlights the potential for opioid-based therapies in mitigating IRI-induced myocardial damage.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811529","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

IL-22 Attenuates Pressure Overload-Induced Heart Failure and Inflammation. IL-22减轻压力过载引起的心力衰竭和炎症。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-07 DOI: 10.1007/s12265-025-10613-2

Lanqing Xiang, Guoqing Yin, Zifan Gong, Xian Lv, Cailin Feng, Lu Liu, Fuad A Abdu, Tingting Shi, Wen Zhang, Jiasuer Alifu, Xiaojiang Xu, Yuxiang Dai, Wenliang Che, Xinyu Weng

引用次数: 0

Association Between Magnesium Depletion Score and Peripheral Artery Disease in Middle-Aged and Older Population. 中老年人群镁耗尽评分与外周动脉疾病的关系

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-07 DOI: 10.1007/s12265-025-10615-0

Zongao Cai, Jiachen She

引用次数: 0

Mesenchymal Stem Cell-based Apelin Gene Therapy Improves Pulmonary Artery Remodeling in Monocrotaline-induced Pulmonary Hypertension Through PI3K/AKT/eNOS and ERK1/2 Signaling Pathways. 基于间充质干细胞的Apelin基因治疗通过PI3K/AKT/eNOS和ERK1/2信号通路改善单芥碱诱导的肺动脉高压的肺动脉重塑

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-04-01 DOI: 10.1007/s12265-025-10612-3

Li Wang, Weijian Wang, Ting Wu, Liang Chen, Gangjun Zong

{"title":"Mesenchymal Stem Cell-based Apelin Gene Therapy Improves Pulmonary Artery Remodeling in Monocrotaline-induced Pulmonary Hypertension Through PI3K/AKT/eNOS and ERK1/2 Signaling Pathways.","authors":"Li Wang, Weijian Wang, Ting Wu, Liang Chen, Gangjun Zong","doi":"10.1007/s12265-025-10612-3","DOIUrl":"https://doi.org/10.1007/s12265-025-10612-3","url":null,"abstract":"Pulmonary arterial hypertension (PAH) poses a challenge due to limited curative options and ineffective treatments. Mesenchymal stem cell (MSC) therapy has emerged as a potential intervention for PAH. This study delved into the therapeutic potential and molecular mechanisms underlying MSC-based apelin gene therapy in PAH rats induced by monocrotaline (MCT). Wharton's jelly-derived MSCs transfected with pcSLenti-APLN were utilized as therapeutic agents. Transplanted MSCs successfully homed to the lung tissue of rats and sustained survival for at least three weeks. MSC-mediated apelin gene therapy effectively reduced pulmonary artery pressure, mitigated pulmonary vascular remodeling, and modulated apoptosis in MCT-induced PAH rats. Furthermore, the phosphatidylinositol 3-kinase (PI3K)/AKT/endothelial nitric oxide synthase (eNOS) and ERK1/2 signaling pathways were involved in the therapeutic effects. Meanwhile, Apelin-MSCs also regulated MCT-induced changes of Bax and Bcl-2 in the lung lobes and pulmonary arterioles. MSC-based apelin gene therapy could be considered a possible therapeutic strategy for PAH.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752870","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 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

RNA Therapies in Cardio-Kidney-Metabolic Syndrome: Advancing Disease Management. 心肾代谢综合征的RNA治疗：推进疾病管理。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2025-03-13 DOI: 10.1007/s12265-025-10603-4

Abbas Mohammadi, Azin Karimian, Kasra Shokri, Ashkan Mohammadi, Nazanin Hazhir-Karzar, Rayeheh Bahar, Azar Radfar, Mohammadreza Pakyari, Behnam Tehrani

{"title":"RNA Therapies in Cardio-Kidney-Metabolic Syndrome: Advancing Disease Management.","authors":"Abbas Mohammadi, Azin Karimian, Kasra Shokri, Ashkan Mohammadi, Nazanin Hazhir-Karzar, Rayeheh Bahar, Azar Radfar, Mohammadreza Pakyari, Behnam Tehrani","doi":"10.1007/s12265-025-10603-4","DOIUrl":"https://doi.org/10.1007/s12265-025-10603-4","url":null,"abstract":"Cardio-Kidney-Metabolic (CKM) Syndrome involves metabolic, kidney, and cardiovascular dysfunction, disproportionately affecting disadvantaged groups. Its staging (0-4) highlights the importance of early intervention. While current management targets hypertension, heart failure, dyslipidemia, and diabetes, RNA-based therapies offer innovative solutions by addressing molecular mechanisms of CKM Syndrome. Emerging RNA treatments, including antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs), show promise in slowing disease progression across CKM stages. For example, ASOs and siRNAs targeting ApoC-III and ANGPTL3 reduce triglycerides and LDL cholesterol, while siRNAs improve blood pressure control by targeting the renin-angiotensin-aldosterone system. Obesity treatments leveraging miRNAs and circRNAs tackle a key CKM risk factor. In heart failure and diabetes, RNA-based therapies improve cardiac function and glucose control, while early kidney disease trials show potential for RNAi in acute injury. Further research is essential to refine these therapies and ensure equitable access.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624877","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