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Journal of Cardiovascular Translational Research最新文献

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SLC11A1 Drives Ferroptosis in Acute Myocardial Infarction Via Sp1-mediated Transcriptional Repression of GPX4. SLC11A1通过sp1介导的GPX4转录抑制驱动急性心肌梗死的铁凋亡。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-06-03 DOI: 10.1007/s12265-026-10782-8
Shirong Zhang, Yeshu Wang, Yangmei Feng, Fang Wang, Jiaqing Zhu
{"title":"SLC11A1 Drives Ferroptosis in Acute Myocardial Infarction Via Sp1-mediated Transcriptional Repression of GPX4.","authors":"Shirong Zhang, Yeshu Wang, Yangmei Feng, Fang Wang, Jiaqing Zhu","doi":"10.1007/s12265-026-10782-8","DOIUrl":"10.1007/s12265-026-10782-8","url":null,"abstract":"<p><p>Ferroptosis is a critical contributor to cardiomyocyte injury in acute myocardial infarction (AMI). This study aimed to identify key ferroptosis-associated genes and elucidate their roles in AMI. Transcriptomic datasets from AMI patients and healthy controls were analyzed to identify differentially expressed genes (DEGs). The role of the solute carrier family 11 member 1 (SLC11A1) was validated in vitro using a hypoxia/reoxygenation (H/R) model in H9c2 cardiomyocytes and in vivo using a murine AMI model. SLC11A1 expression was elevated in H/R-treated cardiomyocytes and infarcted murine hearts. SLC11A1 silencing reduced infarct size and improved cardiac function, and suppressed ferroptosis. Mechanistically, SLC11A1 led to the transcriptional suppression of glutathione peroxidase 4 (GPX4) mediated by the transcription factor specificity protein 1 (Sp1). This study identifies the SLC11A1-Sp1-GPX4 axis as a pivotal transcriptional regulator pathway driving ferroptosis in AMI. These findings highlight SLC11A1 as a promising therapeutic target in AMI.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148149915","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
Transjugular Transcatheter Tricuspid Valve Implantation of Coronary Stent System for Creating a Rat Tricuspid Regurgitation Model. 经颈静脉经导管三尖瓣植入冠状动脉支架系统建立大鼠三尖瓣反流模型。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-06-03 DOI: 10.1007/s12265-026-10790-8
Xiaoping Ning, Hongjie Xu, Quangong Zhao, Jiajun Pan, Xiaohong Liu, Jingyi Cao, Qin Li, Sufan Ding, Chao Ye, Keng Zhong, Shangyi Yu, Fanglin Lu, Lin Han, Zhiyun Xu, Fan Qiao
{"title":"Transjugular Transcatheter Tricuspid Valve Implantation of Coronary Stent System for Creating a Rat Tricuspid Regurgitation Model.","authors":"Xiaoping Ning, Hongjie Xu, Quangong Zhao, Jiajun Pan, Xiaohong Liu, Jingyi Cao, Qin Li, Sufan Ding, Chao Ye, Keng Zhong, Shangyi Yu, Fanglin Lu, Lin Han, Zhiyun Xu, Fan Qiao","doi":"10.1007/s12265-026-10790-8","DOIUrl":"10.1007/s12265-026-10790-8","url":null,"abstract":"<p><p>We aimed to establish a rat TR model to further investigate the mechanisms of right heart remodeling and organ damage induced by TR. Intervention group rats (n = 6) underwent coronary stent system implantation via transjugular approach. The control group (n = 6) underwent the same procedure, except for coronary stent implantation. All rats survived at 8 weeks follow-up postoperatively. TR occurred immediately after the implantation of coronary stent in the intervention group. The right ventricular fractional area change (FAC) decreased by 33.9% compared with baseline from 0.59 ± 0.11% to 0.39 ± 0.10% (P = 0.005) and the tricuspid annular plane systolic excursion (TAPSE) decreased by 36.8% from 2.42 ± 0.31 mm to 1.53 ± 0.45 mm at 8 weeks (P < 0.001). This animal model would be suitable to further investigate the mechanisms of right ventricular remodeling and other organ damage associated with TR.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148149905","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
Beyond the Powerhouse: Mitochondrial Crosstalk as a Master Regulator of Cardiac Metabolic Homeostasis and Failure. 超越动力：线粒体串扰作为心脏代谢稳态和衰竭的主要调节因子。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-05-28 DOI: 10.1007/s12265-026-10776-6
Yu-Xin Kang, Yue Hu, Xi-Tong Sun, Xin-Biao Fan, Ao-Lin Li, Wen-Yu Shang, Yun-Feng Jia, Yi-Xuan Zhao, Miao-Miao Wei, Tian-Qi Wang, Zheng Zhang, Bo-Yu Zhu, Yong-Chun Liang, Jun-Ping Zhang
{"title":"Beyond the Powerhouse: Mitochondrial Crosstalk as a Master Regulator of Cardiac Metabolic Homeostasis and Failure.","authors":"Yu-Xin Kang, Yue Hu, Xi-Tong Sun, Xin-Biao Fan, Ao-Lin Li, Wen-Yu Shang, Yun-Feng Jia, Yi-Xuan Zhao, Miao-Miao Wei, Tian-Qi Wang, Zheng Zhang, Bo-Yu Zhu, Yong-Chun Liang, Jun-Ping Zhang","doi":"10.1007/s12265-026-10776-6","DOIUrl":"10.1007/s12265-026-10776-6","url":null,"abstract":"<p><p>Mitochondrial dysfunction has long been recognized as a central driver of heart failure (HF) pathogenesis, and emerging evidence highlights that impaired mitochondrial communication, rather than merely energy metabolism dysfunction, plays a pivotal role in the initiation and progression of HF. These communication networks are critical for maintaining cardiac metabolic homeostasis, and their disruption in HF leads to dysregulated energy metabolism, oxidative stress, lipotoxicity, and impaired cardiomyocyte function. This review examines the functional interactions between mitochondria and these organelles in HF, with particular attention to phenotype-specific differences between HF with preserved ejection fraction and HF with reduced ejection fraction. Finally, we summarize current and emerging therapeutic strategies targeting mitochondrial communication, highlighting the potential for phenotype-tailored interventions that restore organelle interplay and metabolic balance in HF.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148054654","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
Metabolic Remodeling Induced by Exercise: Emerging Mechanisms for Myocardial Protection in Cardiovascular Disease. 运动诱导的代谢重塑：心血管疾病心肌保护的新机制
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-05-27 DOI: 10.1007/s12265-026-10781-9
Tianwen Wei, Chang Zhou, Jieyun You, Yuxiao Sun, Qi Zhang
{"title":"Metabolic Remodeling Induced by Exercise: Emerging Mechanisms for Myocardial Protection in Cardiovascular Disease.","authors":"Tianwen Wei, Chang Zhou, Jieyun You, Yuxiao Sun, Qi Zhang","doi":"10.1007/s12265-026-10781-9","DOIUrl":"10.1007/s12265-026-10781-9","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs), including coronary artery disease, heart failure, arrhythmias, hypertension, and cardiomyopathy, promote disease progression in part through profound disturbances in cardiomyocyte metabolism. These disorders are characterized by abnormal lipid and glucose metabolism and dysfunction of key metabolic regulatory systems, including fatty acid transport proteins and the AMPK/eNOS signaling axis. Exercise training regulates substrate selection and activates essential metabolic pathways, including PGC-1α and PPAR-α, thereby improving myocardial energy homeostasis and limiting cardiac injury. This review summarizes the mechanisms by which exercise modulates myocardial metabolism to delay or reverse disease progression across multiple forms of CVDs. Current evidence indicates that distinct cardiovascular pathologies exhibit unique metabolic abnormalities, suggesting that exercise interventions may exert disease-specific therapeutic effects by selectively targeting altered metabolic pathways.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148030885","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
Towards Neoatherosclerosis: A Porcine Model for Enhanced Device Testing. 迈向新动脉粥样硬化：用于增强器械检测的猪模型。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-05-26 DOI: 10.1007/s12265-026-10778-4
Jing Xie, Ole Gemeinhardt, Stephanie Bettink, Ralf Hauptmann, Mathias Schannor, Melanie Loechel, Ulrich Speck, Tobias Haase
{"title":"Towards Neoatherosclerosis: A Porcine Model for Enhanced Device Testing.","authors":"Jing Xie, Ole Gemeinhardt, Stephanie Bettink, Ralf Hauptmann, Mathias Schannor, Melanie Loechel, Ulrich Speck, Tobias Haase","doi":"10.1007/s12265-026-10778-4","DOIUrl":"10.1007/s12265-026-10778-4","url":null,"abstract":"<p><p>The porcine in-stent stenosis model has been essential for developing drug-coated devices but does not replicate the hyperlipidemic, pro-atherogenic conditions driving neoatherosclerosis. We aimed to establish a practical porcine model for testing endovascular therapies targeting neoatherosclerosis. Juvenile pigs were fed a high-fat, nicotine-supplemented diet (HFDN). After two weeks, bare-metal stents were implanted in coronary and peripheral arteries; controls received a standard diet. Four weeks later, stented, and non-stented artery segments were analyzed. HFDN feeding induced elevated serum LDL and cotinine. At follow-up, in-stent late lumen loss was significantly greater in peripheral arteries (A. iliaca: 2.3 ± 0.6 vs. 1.1 ± 0.5 mm; A. femoralis: 3.4 ± 1.2 vs. 2.0 ± 0.4 mm), but not coronary arteries. HFDN-fed pigs showed distinct signs of early neoatherosclerosis, including peri-strut foam cell accumulations and atheroma formation. Elemental imaging and chemical analysis confirmed increased calcium phosphate deposition in arteries of HFDN-fed pigs. This straightforward protocol enables testing of devices aimed at preventing or treating neoatherosclerosis.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13212638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148031063","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
Comment on "Pressure Measurements Obtained From Intraosseous Access: Potential Clinical Applications Explored Using a Porcine Model". 对“从骨内通道获得的压力测量：利用猪模型探索潜在的临床应用”的评论。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-05-26 DOI: 10.1007/s12265-026-10785-5
Neeraj Singh, Monika Srivastav
{"title":"Comment on \"Pressure Measurements Obtained From Intraosseous Access: Potential Clinical Applications Explored Using a Porcine Model\".","authors":"Neeraj Singh, Monika Srivastav","doi":"10.1007/s12265-026-10785-5","DOIUrl":"10.1007/s12265-026-10785-5","url":null,"abstract":"","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148030911","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
Psychological Scars and Physical Consequences: Linking PTSD to Cardiovascular Health. 心理创伤和生理后果：创伤后应激障碍与心血管健康的联系。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-05-26 DOI: 10.1007/s12265-026-10783-7
Alexa Corker, Griffin Oh, Kristine Y DeLeon-Pennell
{"title":"Psychological Scars and Physical Consequences: Linking PTSD to Cardiovascular Health.","authors":"Alexa Corker, Griffin Oh, Kristine Y DeLeon-Pennell","doi":"10.1007/s12265-026-10783-7","DOIUrl":"10.1007/s12265-026-10783-7","url":null,"abstract":"<p><p>Post traumatic stress disorder (PTSD) is defined as a mental health condition that occurs after experiencing a traumatic event. Patients diagnosed with PTSD have a 30-45% increase in cardiovascular disease (CVD) risk or cardiac-specific mortality even after adjusting for depression, demographic, clinical (e.g., age, blood pressure, body mass index (BMI), and tobacco use), and psychosocial factors. With this, the lifetime prevalence of PTSD has a notable sex disparity: women have a prevalence of approximately 10%, compared to 4% in men. Mechanisms explaining the increased risk of CVD in PTSD patients is unclear, leaving this patient population vulnerable as well as placing a substantial economic burden on the United States healthcare system. In this review, we will discuss the effect of PTSD on cardiovascular physiology, with an emphasis on sex differences, mechanisms of inflammation, and impaired ANS responses. In addition, we will summarize current and experimental therapeutics for PTSD that may help mitigate the risk of CVD.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13212789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148031043","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
Persistent Proteomic Signatures in Takotsubo Syndrome: Methodological Considerations Regarding Reference Cohort Selection and Confounding. Takotsubo综合征的持续蛋白质组学特征：关于参考队列选择和混淆的方法学考虑。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-05-26 DOI: 10.1007/s12265-026-10786-4
Fatih Aydin
{"title":"Persistent Proteomic Signatures in Takotsubo Syndrome: Methodological Considerations Regarding Reference Cohort Selection and Confounding.","authors":"Fatih Aydin","doi":"10.1007/s12265-026-10786-4","DOIUrl":"10.1007/s12265-026-10786-4","url":null,"abstract":"","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148030985","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
Iron Deficiency Screening in Patients Admitted with Acute Heart Failure Decompensation. 急性心力衰竭失代偿患者的缺铁筛查。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-05-19 DOI: 10.1007/s12265-026-10774-8
Alex M Sindledecker, Yassar Nabeel, Olivia Palladino, Lawrence A Frazee
{"title":"Iron Deficiency Screening in Patients Admitted with Acute Heart Failure Decompensation.","authors":"Alex M Sindledecker, Yassar Nabeel, Olivia Palladino, Lawrence A Frazee","doi":"10.1007/s12265-026-10774-8","DOIUrl":"10.1007/s12265-026-10774-8","url":null,"abstract":"<p><p>Correction of iron deficiency (ID) with intravenous iron among patients with heart failure (HF) may improve outcomes but is rarely assessed in real-world studies. Hospital admission for decompensated HF presents an opportunity to identify patients for treatment of ID. Of 2,275 patient admissions for decompensated HF, iron studies were available for 526 (23.1%) and ID was identified in 332 (63.1%) patients. Iron replacement was oral in 241 (10.6%) or intravenous in 285 (12.5%) with 132 (46.3%) patients receiving treatment during the admission. Anemia, chronic kidney disease stage 3 (CKD3), and low mean corpuscular volume (MCV) were associated with a higher odds of iron study availability while age was associated with lower odds. Frequency of assessment of ID in HF patients remains low. Predictors of iron status assessment indicate that factors related to anemia rather than HF are likely responsible for iron status assessment among these patients.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13186904/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972835","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
Xanthatin Attenuates Angiotensin II-Induced Cardiac Hypertrophy by Targeting CREB5. 黄嘌呤通过靶向CREB5减轻血管紧张素ii诱导的心肌肥厚。
IF 2.6 3区 医学
Journal of Cardiovascular Translational Research Pub Date : 2026-05-19 DOI: 10.1007/s12265-026-10777-5
Xiang-Bo An, Yi-Tong Wang, Xin Liu, Fei Gao, Zhi-Jian Wang
{"title":"Xanthatin Attenuates Angiotensin II-Induced Cardiac Hypertrophy by Targeting CREB5.","authors":"Xiang-Bo An, Yi-Tong Wang, Xin Liu, Fei Gao, Zhi-Jian Wang","doi":"10.1007/s12265-026-10777-5","DOIUrl":"10.1007/s12265-026-10777-5","url":null,"abstract":"<p><p>Pathological cardiac hypertrophy is a key precursor to heart failure. The role of Xanthatin in this process was unknown. This study aimed to investigate its effects and molecular target. A mouse model of Ang II-induced hypertrophy was used. Xanthatin's effects were assessed by echocardiography and histology. Cardiac-specific overexpression or knockdown of CREB5 was performed using AAV9-cTNT vectors during Ang II and Xanthatin co-treatment to validate its functional role. Xanthatin treatment significantly alleviated Ang II-induced cardiac hypertrophy, oxidative stress, fibrosis, and inflammation. Crucially, cardiac-specific overexpression of CREB5 markedly attenuated these protective effects of Xanthatin. Conversely, cardiac-specific knockdown of CREB5 synergized with Xanthatin, further enhancing its suppressive actions on all pathological hallmarks. Xanthatin is a potent inhibitor of Ang II-induced cardiac hypertrophy, and its protective effect is mediated through the suppression of CREB5 signaling. This identifies the Xanthatin-CREB5 axis as a novel and promising therapeutic target for pathological cardiac remodeling.</p>","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972832","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
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