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

Integrated Bioinformatics and Experimental Validation of Post-Translational Modification-Related Biomarkers in Myocardial Ischemia-Reperfusion Injury. 心肌缺血再灌注损伤中翻译后修饰相关生物标志物的综合生物信息学和实验验证。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-08-12 DOI: 10.1007/s12265-026-10821-4

Rina Jiang, Yuefeng Li, Kehan Chen, Xiaoping Chen, Yan Liu, Peng Liang, Zhaohe Huang

{"title":"Integrated Bioinformatics and Experimental Validation of Post-Translational Modification-Related Biomarkers in Myocardial Ischemia-Reperfusion Injury.","authors":"Rina Jiang, Yuefeng Li, Kehan Chen, Xiaoping Chen, Yan Liu, Peng Liang, Zhaohe Huang","doi":"10.1007/s12265-026-10821-4","DOIUrl":"10.1007/s12265-026-10821-4","url":null,"abstract":"Myocardial ischemia-reperfusion injury (MIRI) lacks fully established post-translational modification (PTM)-associated biomarkers. This study aimed to identify and validate PTM-related MIRI biomarkers through integrated bioinformatics analyses and in vitro experiments. RNA-sequencing datasets were analyzed using weighted gene co-expression network analysis (WGCNA), which identified a brown module strongly associated with the MIRI phenotype. Intersection analysis was performed among the brown gene module, differentially expressed genes, and post-translational modification-related gene sets, two core candidate genes, Myc and Rnf115, were ultimately selected. Both genes demonstrated high diagnostic potential in receiver operating characteristic analyses and exhibited positive correlations with dendritic cell and macrophage infiltration, indicating roles in immune modulation. Hypoxia/reoxygenation assays using H9C2 rat cardiomyocytes confirmed the upregulation of Myc and Rnf115 during early MIRI, aligning with bioinformatics trends. Consequently, Myc and Rnf115 were identified as promising PTM-associated biomarkers potentially involved in MIRI pathogenesis.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148725974","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

Nicotinamide Mononucleotide Ameliorates Myocardial Fibrosis in Diabetic Mice Possibly by Modulating SIRT3 to Deacetylate GSK3β and Thereby Reducing the Phosphorylation of Smad3. 烟酰胺单核苷酸可能通过调节SIRT3使GSK3β去乙酰化从而降低Smad3的磷酸化来改善糖尿病小鼠的心肌纤维化。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-08-10 DOI: 10.1007/s12265-026-10827-y

Zuowang Ma, Liyang Yao, Kai Zhang, Yu Yang

{"title":"Nicotinamide Mononucleotide Ameliorates Myocardial Fibrosis in Diabetic Mice Possibly by Modulating SIRT3 to Deacetylate GSK3β and Thereby Reducing the Phosphorylation of Smad3.","authors":"Zuowang Ma, Liyang Yao, Kai Zhang, Yu Yang","doi":"10.1007/s12265-026-10827-y","DOIUrl":"10.1007/s12265-026-10827-y","url":null,"abstract":"This study aims to investigate the therapeutic potential of NMN in alleviating type 2 diabetes-induced myocardial fibrosis.The experiment was comprised of control group, diabetic group, DM + NMN intervention group, and DM + NMN+3-TYP group. Blood glucose level, tibia length, cardiac function, myocardial interstitial fibrosis and ROS level were evaluated. The expression of SIRT3, GSK3β, ac-GSK3β, downstream fibrosis-related proteins and the interaction between SIRT3 and GSK3β were analyzed. Diabetic mice exhibited pronounced myocardial interstitial fibrosis alongside significant alterations in cardiac structure and function. Additionally, the protein expression levels of ac-GSK3β/GSK3β, p-Smad3/t-Smad3, α-SMA, and Collagen I were elevated, while SIRT3 expression was reduced. NMN effectively ameliorated these changes. The therapeutic benefits of NMN were effectively inhibited by 3-TYP. NMN effectively combats diabetes-induced myocardial fibrosis, potentially through upregulating SIRT3 expression. This upregulation may enhance the interaction between SIRT3 and GSK3β, thereby reducing the acetylation of GSK3β. Through this mechanism, NMN ultimately suppresses Smad3 phosphorylation.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148701317","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

Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis. 运动预处理激活AMPK-ACC信号并减轻心肌缺血/再灌注诱导的铁下垂。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-08-07 DOI: 10.1007/s12265-026-10828-x

Yuxiang Xu, Jie Tang, Chenyang Wu, Ruizhen Li, Yifang Zhao, Mengxin Cai, Zhenjun Tian

{"title":"Exercise Preconditioning Activates AMPK-ACC Signaling and Attenuates Myocardial Ischemia/Reperfusion-Induced Ferroptosis.","authors":"Yuxiang Xu, Jie Tang, Chenyang Wu, Ruizhen Li, Yifang Zhao, Mengxin Cai, Zhenjun Tian","doi":"10.1007/s12265-026-10828-x","DOIUrl":"10.1007/s12265-026-10828-x","url":null,"abstract":"Ferroptosis critically mediates myocardial ischemia/reperfusion (I/R) injury. Exercise training confers cardioprotection, but whether it protects against I/R-induced ferroptosis and the underlying mechanisms remain unclear. In this study, C57BL/6J mice underwent six weeks of treadmill exercise preconditioning (EP) before myocardial I/R induction. Cardiac function, oxidative stress, ferroptosis markers and the phosphorylation of AMPK and ACC were assessed. In vitro, H9C2 cells were subjected to hypoxia/reoxygenation (H/R), and pharmacological modulators were used to investigate the necessity of the AMPK-ACC signaling. Results showed that EP alleviated I/R-induced cardiac dysfunction, reduced oxidative stress and iron deposition, upregulated GPX4 and SLC7A11 expression, downregulated ACSL4 expression, and enhanced the phosphorylation of AMPK and ACC. In H9C2 cells, H/R reduced ACC phosphorylation and induced ferroptosis. AMPK inhibition exacerbated H/R-induced ferroptosis, whereas AMPK activation by AICAR was protective. Critically, blocking ACC enzymatic activity attenuated AICAR's effects. These findings indicate that EP attenuates I/R-induced ferroptosis and the AMPK-ACC signaling may contribute to this protective effect.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684602","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

Empagliflozin Improves Endothelial Function in an Ovariectomized Rat Model of Estrogen Deficiency. 恩格列净改善雌激素缺乏大鼠去卵巢模型的内皮功能。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-08-06 DOI: 10.1007/s12265-026-10823-2

Amanina Athirah Mad Azli, Mohd Helmy Mokhtar, Amilia Aminuddin, Adila A Hamid, Jaya Kumar, Mohd Faizal Ahmad, Azizah Ugusman

{"title":"Empagliflozin Improves Endothelial Function in an Ovariectomized Rat Model of Estrogen Deficiency.","authors":"Amanina Athirah Mad Azli, Mohd Helmy Mokhtar, Amilia Aminuddin, Adila A Hamid, Jaya Kumar, Mohd Faizal Ahmad, Azizah Ugusman","doi":"10.1007/s12265-026-10823-2","DOIUrl":"10.1007/s12265-026-10823-2","url":null,"abstract":"Cardiovascular disease risk increases after menopause, largely driven by estrogen deficiency-induced endothelial dysfunction. While sodium-glucose cotransporter 2 (SGLT2) inhibitors confer cardiovascular protection, their vascular effects under estrogen-deficient conditions remain unclear. This study investigated the effects of the SGLT2 inhibitor empagliflozin on vascular function in an ovariectomized (OVX) rat model of estrogen deficiency. Female Sprague-Dawley rats were assigned to control, OVX, OVX + vehicle, OVX + empagliflozin (10 mg/kg/day), and OVX + estradiol (20 µg/kg/day) groups for 28 days. Vascular reactivity was assessed using wire myography, alongside evaluation of endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) levels. OVX rats exhibited impaired endothelium-dependent vasorelaxation, increased vasoconstriction, reduced eNOS activation, and decreased NO bioavailability. Empagliflozin significantly improved vascular reactivity, enhanced eNOS activation, and restored NO levels, with effects comparable to estradiol. These findings identify empagliflozin as a potential non-hormonal therapeutic strategy for endothelial dysfunction in postmenopausal conditions.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148684570","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

Timing and Duration of Prediabetic Metabolic Dysfunction Differentially Impact Cerebral Perfusion, Vascular Structure, and Behavior. 糖尿病前期代谢功能障碍的时间和持续时间对脑灌注、血管结构和行为的差异影响。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-08-05 DOI: 10.1007/s12265-026-10806-3

Annika Matthiesen, Stephanie DiLucia, Riley Feagle, Sadie Lofton, Isabel Marshall, Catrina Robinson, Adviye Ergul

{"title":"Timing and Duration of Prediabetic Metabolic Dysfunction Differentially Impact Cerebral Perfusion, Vascular Structure, and Behavior.","authors":"Annika Matthiesen, Stephanie DiLucia, Riley Feagle, Sadie Lofton, Isabel Marshall, Catrina Robinson, Adviye Ergul","doi":"10.1007/s12265-026-10806-3","DOIUrl":"10.1007/s12265-026-10806-3","url":null,"abstract":"Obesity is a major risk factor for metabolic dysfunction and cognitive decline, yet the influence of age of onset and sex on neurovascular outcomes remains unclear. We examined how the age at initiation and duration of diet-induced obesity influence metabolism, cognition, and cerebrovascular perfusion in male and female mice. A high-fat diet increased body weight and impaired glucose regulation, particularly in females. Obesity selectively impaired recognition memory while sparing spatial working memory. Cerebrovascular effects were region- and age-specific. Early- and mid-life obesity produced localized perfusion changes despite preserved global cortical blood flow. In contrast, early-life obesity was associated with reduced cortical perfusion and decreased hippocampal vascular complexity, including fewer branch points and smaller vessel diameters. These alterations parallel recognition memory deficits, suggesting a vascular mechanism linking early metabolic stress to cognitive impairment. Together, our findings identify early-life obesity as a critical window of vulnerability for long-term neurovascular and cognitive dysfunction.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":"19 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13442511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678787","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

Exercise-Induced Regulation of LncRNAs: Mechanistic Insights and Clinical Translation in Cardiovascular Health. 运动诱导的lncrna调控：心血管健康的机制见解和临床翻译。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-08-05 DOI: 10.1007/s12265-026-10829-w

Tao Gao, Li-Hua Yu

引用次数: 0

Beyond the Pump: Unravelling Immunometabolic Crosstalk and Organelle Dynamics in Sepsis-Induced Cardiomyopathy. 在泵之外：在败血症引起的心肌病中解开免疫代谢串扰和细胞器动力学。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-08-04 DOI: 10.1007/s12265-026-10826-z

Guangfu Liu, Liya Hao, Junfeng Zhang, Yidan Guo, Guangyue Lv, Jiuyuan Liu, Cheng Cheng, Han Yi, Jingjing Zhou, Zhenzhu Liu

引用次数: 0

Autoantibody-Based Models for the Diagnosis and Activity Assessment of Takayasu Arteritis. 基于自身抗体的高须动脉炎诊断和活动性评估模型。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-08-03 DOI: 10.1007/s12265-026-10824-1

Jianxiong Wu, Jing Cui, Fengjuan Li, Xin Tan, Xue Wang, Yuan Wang

引用次数: 0

FOSL2 Regulates PANoptosis in Cardiomyocytes and Heart Failure Progression After Acute Myocardial Infarction by Promoting NLRP12. FOSL2通过促进NLRP12调节急性心肌梗死后心肌细胞PANoptosis和心力衰竭进展。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-07-28 DOI: 10.1007/s12265-026-10819-y

Renlian Gu, Yan Sun

引用次数: 0

Small Animal Models for Translational Research in Atrial Fibrillation. 房颤转化研究的小动物模型。

IF 2.6 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2026-07-20 DOI: 10.1007/s12265-026-10817-0

Yunmeng Wang, Jiaqi Wang, Yawei Liu, Jingchao Lu

引用次数: 0