Journal of Cardiovascular Translational Research最新文献_第3页

CD137 Signaling Mediates Pulmonary Artery Endothelial Cell Proliferation Under Hypoxia By Regulating Mitochondrial Dynamics. CD137 信号通过调节线粒体动力学介导缺氧条件下肺动脉内皮细胞增殖

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 Epub Date: 2024-02-12 DOI: 10.1007/s12265-024-10493-y

Hao Xia, Junying Duan, Mei Li, Nan Chen, Wei Zhong, Ye Zhou, Rui Chen, Wei Yuan

{"title":"CD137 Signaling Mediates Pulmonary Artery Endothelial Cell Proliferation Under Hypoxia By Regulating Mitochondrial Dynamics.","authors":"Hao Xia, Junying Duan, Mei Li, Nan Chen, Wei Zhong, Ye Zhou, Rui Chen, Wei Yuan","doi":"10.1007/s12265-024-10493-y","DOIUrl":"10.1007/s12265-024-10493-y","url":null,"abstract":"Altered mitochondrial dynamics affect pulmonary artery endothelial cells (PAECs) proliferation, contributing to the development of pulmonary hypertension. CD137 signaling promotes mitochondrial fission. We hypothesize CD137 signaling is involved in the excessive proliferation of PAECs. The levels of CD137 protein were increased in the lung tissue of hypoxic mice and hypoxic-stimulated PAECs. Activation of CD137 signal in hypoxic-PAECs upregulated the levels of hypoxia-inducible factor-2α (HIF-2α), glucose transporters type 4, the lactate transporter monocarboxylate transporter 4, key glycolysis rate-limiting enzymes and promoted mitochondrial division; moreover, increased glucose uptake, lactic acid and ATP production and proliferative cells were observed in these PAECs. Whereas, knockdown HIF-2α reversed CD137 signal-mediated effects in PAECs mentioned above. Compared with wild-type mice, the proliferation of PAECs and the percentage of vascular lateral wall thickness decreased in CD137 knockout mice. Together, CD137 signal participated in pulmonary vascular remodeling through the regulation of mitochondrial dynamics dependent on HIF-2α in PAECs.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722800","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

Association Between Automated 3D Measurement of Coronary Luminal Narrowing and Risk of Future Myocardial Infarction. 冠状动脉管腔狭窄自动三维测量与未来心肌梗死风险之间的关系

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 Epub Date: 2024-03-01 DOI: 10.1007/s12265-024-10500-2

Alessandro Candreva, Maurizio Lodi Rizzini, Karol Calò, Mattia Pagnoni, Daniel Munhoz, Claudio Chiastra, Jean-Paul Aben, Stephane Fournier, Olivier Muller, Bernard De Bruyne, Carlos Collet, Diego Gallo, Umberto Morbiducci

{"title":"Association Between Automated 3D Measurement of Coronary Luminal Narrowing and Risk of Future Myocardial Infarction.","authors":"Alessandro Candreva, Maurizio Lodi Rizzini, Karol Calò, Mattia Pagnoni, Daniel Munhoz, Claudio Chiastra, Jean-Paul Aben, Stephane Fournier, Olivier Muller, Bernard De Bruyne, Carlos Collet, Diego Gallo, Umberto Morbiducci","doi":"10.1007/s12265-024-10500-2","DOIUrl":"10.1007/s12265-024-10500-2","url":null,"abstract":"This study focuses on identifying anatomical markers with predictive capacity for long-term myocardial infarction (MI) in focal coronary artery disease (CAD). Eighty future culprit lesions (FCL) and 108 non-culprit lesions (NCL) from 80 patients underwent 3D quantitative coronary angiography. The minimum lumen area (MLA), minimum lumen ratio (MLR), and vessel fractional flow reserve (vFFR) were evaluated. MLR was defined as the ratio between MLA and the cross-sectional area at the proximal lesion edge, with lower values indicating more abrupt luminal narrowing. Significant differences were observed between FCL and NCL in MLR (0.41 vs. 0.53, p < 0.001). MLR correlated inversely with translesional vFFR (r = - 0.26, p = 0.0004) and was the strongest predictor of MI at 5 years (AUC = 0.75). Lesions with MLR < 0.40 had a fourfold increased MI incidence at 5 years. MLR is a robust predictor of future adverse coronary events.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11371893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139996326","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

Reply to Correspondence on "Absence of Myocardial Involvement after SARS-CoV-2 Vaccination in Asymptomatic Adolescents". 对有关 "无症状青少年接种 SARS-CoV-2 疫苗后心肌未受感染 "的来函的答复

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 Epub Date: 2024-02-13 DOI: 10.1007/s12265-024-10492-z

Rocío Párraga, Carlos Real, Rodrigo Fernández-Jiménez

引用次数: 0

Lipoamide Attenuates Hypertensive Myocardial Hypertrophy Through PI3K/Akt-Mediated Nrf2 Signaling Pathway. 脂酰胺通过PI3K/Akt介导的Nrf2信号通路减轻高血压性心肌肥厚

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 Epub Date: 2024-02-09 DOI: 10.1007/s12265-024-10488-9

Hongjuan Cao, Lina Zhao, Yao Yuan, Chunyan Liao, Weidan Zeng, Aiyue Li, Quanfeng Huang, Yueyao Zhao, Yubing Fan, Liu Jiang, Dandan Song, Sha Li, Bei Zhang

{"title":"Lipoamide Attenuates Hypertensive Myocardial Hypertrophy Through PI3K/Akt-Mediated Nrf2 Signaling Pathway.","authors":"Hongjuan Cao, Lina Zhao, Yao Yuan, Chunyan Liao, Weidan Zeng, Aiyue Li, Quanfeng Huang, Yueyao Zhao, Yubing Fan, Liu Jiang, Dandan Song, Sha Li, Bei Zhang","doi":"10.1007/s12265-024-10488-9","DOIUrl":"10.1007/s12265-024-10488-9","url":null,"abstract":"The process of myocardial hypertrophy in hypertension can lead to excessive activation of oxidative stress. Lipoamide (ALM) has significant antioxidant and anti-inflammatory effects. This study aimed to investigate the effects of ALM on hypertension-induced cardiac hypertrophy, as well as explore its underlying mechanisms. We evaluated the effects of ALM on spontaneously hypertensive rats and rat cardiomyocytes treated with Ang II. We found that ALM was not effective in lowering blood pressure in SHR, but it attenuated hypertension-mediated cardiac fibrosis, oxidative stress, inflammation, and hypertrophy in rats. After that, in cultured H9C2 cells stimulated with Ang II, ALM increased the expression of antioxidant proteins that were decreased in the Ang II group. ALM also alleviated cell hypertrophy and the accumulation of ROS, while LY294002 partially abrogated these effects. Collectively, these results demonstrate that ALM could alleviate oxidative stress in cardiac hypertrophy, potentially through the activation of the PI3K/Akt-mediated Nrf2 signaling pathway.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11371882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139706852","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

Mzb1 Attenuates Atherosclerotic Plaque Vulnerability in ApoE-/- Mice by Alleviating Apoptosis and Modulating Mitochondrial Function. Mzb1通过缓解细胞凋亡和调节线粒体功能减轻载脂蛋白E-/-小鼠动脉粥样硬化斑块的脆弱性

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 Epub Date: 2024-01-31 DOI: 10.1007/s12265-024-10483-0

Guanglang Zhu, Yang Li, Hongxia Gao, Xu Li, Heyu Fan, Longhua Fan

{"title":"Mzb1 Attenuates Atherosclerotic Plaque Vulnerability in ApoE-/- Mice by Alleviating Apoptosis and Modulating Mitochondrial Function.","authors":"Guanglang Zhu, Yang Li, Hongxia Gao, Xu Li, Heyu Fan, Longhua Fan","doi":"10.1007/s12265-024-10483-0","DOIUrl":"10.1007/s12265-024-10483-0","url":null,"abstract":"In this study, we investigated the protective role of Mzb1 in atherosclerotic plaque vulnerability. To explore the impact of Mzb1, we analyzed Mzb1 expression, assessed apoptosis, and evaluated mitochondrial function in atherosclerosis (AS) mouse models and human vascular smooth muscle cells (HVSMCs). We observed a significant decrease in Mzb1 expression in AS mouse models and ox-LDL-treated HVSMCs. Downregulation of Mzb1 increased ox-LDL-induced apoptosis and cholesterol levels of HVSMCs, while Mzb1 overexpression alleviated these effect. Mzb1 was found to enhance mitochondrial function, as evidenced by restored ATP synthesis, mitochondrial membrane potential, and reduced mtROS production. Moreover, Mzb1 overexpression attenuated atherosclerotic plaque vulnerability in ApoE-/- mice. Our findings suggest that Mzb1 overexpression regulates the AMPK/SIRT1 signaling pathway, leading to the attenuation of atherosclerotic plaque vulnerability. This study provides compelling evidence for the protective effect of Mzb1 on atherosclerotic plaques by alleviating apoptosis and modulating mitochondrial function in ApoE-/- mice.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139642210","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

Therapeutic Strategies for Angiogenesis Based on Endothelial Cell Epigenetics. 基于内皮细胞表观遗传学的血管生成治疗策略。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 Epub Date: 2024-01-31 DOI: 10.1007/s12265-024-10485-y

Yue Cai, Lihua Li, Chen Shao, Yiliu Chen, Zhongqun Wang

引用次数: 0

Changes in Cardiac Electrical Biomarker in Response to Coronary Arterial Occlusion: An Experimental Observation. 冠状动脉闭塞时心脏电生物标志物的变化：实验观察

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 Epub Date: 2024-02-13 DOI: 10.1007/s12265-024-10487-w

Sudipta Chattopadhyay, Felicia Adjei, Attila Kardos

{"title":"Changes in Cardiac Electrical Biomarker in Response to Coronary Arterial Occlusion: An Experimental Observation.","authors":"Sudipta Chattopadhyay, Felicia Adjei, Attila Kardos","doi":"10.1007/s12265-024-10487-w","DOIUrl":"10.1007/s12265-024-10487-w","url":null,"abstract":"Cardiac electrical biomarker (CEB), an indicator of ischaemia-induced change in myocyte polarity, has been proposed for diagnosis of acute coronary syndrome. However, effect of coronary occlusion on CEB has not been demonstrated. CEB was acquired before (CEB0), during maximal adenosine hyperaemia (CEBhyp), balloon inflations (CEBmax) and 1 (CEB1h), 2 (CEB2h) and 3 (CEB3h) h after percutaneous coronary intervention along with pre- and post-procedural troponin-I. CEB of subjects with non-cardiac chest pain without risk factors was used as controls (CEBc). \"Late recovery\" (LR) of CEB was defined as CEB3h > median-CEB0. CEB was recorded in 75 patients undergoing stenting (group 1) including 8 with FFR < 0.8 (group 1a), 25 with FFR ≥ 0.8 (group 2) and 49 controls. In group 1, CEB0 (median, IQR) was higher than CEBc (48.0; 29.5-88.3 vs 30.0; 17.0-44.0; p < 0.001). CEBmax (185; 105.0-331.0) was higher than CEB0 (p < 0.0001). CEB1h (78.0; 31.5-143.8; p < 0.0001) and CEB2h (63.0; 31.5-114.3; p = 0.039) were higher than CEB0 while CEB3h (54.0; 24.3-94.8, p = 0.152) was similar. LR occurred in 50.7% patients. CEBmax predicted LR (OR 1.01, 95% CI 1.00-1.01, p < 0.001) (AUC 0.759, p < 0.001). CEB0 in group 1a and group 2 were similar (p = 0.524). CEBhyp was higher than CEB0 in group 1a (126.0, 109.5-266.0 vs 47.5, 20.5-73.5; p = 0.016) and group 2 (44.0, 27.8-104.8 vs 39.0, 24.0-90.3; p = 0.014). CEBhyp was higher in group 1a than 2 (p = 0.039). CEBhyp (AUC 0.75, p = 0.017) accurately predicted FFR < 0.8. Coronary arterial occlusion increases CEB that retains a \"memory\" of the ischaemic event. CEBhyp was higher only when FFR was ischaemic and accurately identified FFR < 0.8.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139722801","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

Force Analysis Using Self-Expandable Valve Fluoroscopic Imaging: a way Through Artificial Intelligence. 利用自膨胀瓣膜透视成像进行受力分析：一种通过人工智能的方法。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 DOI: 10.1007/s12265-024-10550-6

Yiming Qi, Xiaochun Zhang, Zhiyun Shen, Yixiu Liang, Shasha Chen, Wenzhi Pan, Daxin Zhou, Junbo Ge

引用次数: 0

PPARγ Agonist Rosiglitazone and Antagonist GW9662: Antihypertensive Effects on Chronic Intermittent Hypoxia-Induced Hypertension in Rats. PPARγ 激动剂罗格列酮和拮抗剂 GW9662：对慢性间歇性缺氧诱导的高血压大鼠的降压作用。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 Epub Date: 2024-02-27 DOI: 10.1007/s12265-024-10499-6

Ningzhi Zhang, Feng Wei, Sisi Ning, Jialu Hu, Hongtao Shi, Zhifeng Yao, Minna Tang, Yongqiao Zhang, Jiaxin Gong, Junbo Ge, Zhaoqiang Cui

{"title":"PPARγ Agonist Rosiglitazone and Antagonist GW9662: Antihypertensive Effects on Chronic Intermittent Hypoxia-Induced Hypertension in Rats.","authors":"Ningzhi Zhang, Feng Wei, Sisi Ning, Jialu Hu, Hongtao Shi, Zhifeng Yao, Minna Tang, Yongqiao Zhang, Jiaxin Gong, Junbo Ge, Zhaoqiang Cui","doi":"10.1007/s12265-024-10499-6","DOIUrl":"10.1007/s12265-024-10499-6","url":null,"abstract":"The increased incidence of hypertension associated with obstructive sleep apnea (OSA) presents significant physical, psychological, and economic challenges. Peroxisome proliferator-activated receptor gamma (PPARγ) plays a role in both OSA and hypertension, yet the therapeutic potential of PPARγ agonists and antagonists for OSA-related hypertension remains unexplored. Therefore, we constructed a chronic intermittent hypoxia (CIH)-induced hypertension rat model that mimics the pathogenesis of OSA-related hypertension in humans. The model involved administering PPARγ agonist rosiglitazone (RSG), PPARγ antagonist GW9662, or normal saline, followed by regular monitoring of blood pressure and thoracic aorta analysis using staining and electron microscopy. Intriguingly, our results indicated that both RSG and GW9662 appeared to potently counteract CIH-induced hypertension. In silico study suggested that GW9662's antihypertensive effect might mediated through angiotensin II receptor type 1 (AGTR1). Our findings provide insights into the mechanisms of OSA-related hypertension and propose novel therapeutic targets.","PeriodicalId":15224,"journal":{"name":"Journal of Cardiovascular Translational Research","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139972029","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

Correction: MicroRNA-208a: a Good Diagnostic Marker and a Predictor of no-Reflow in STEMI Patients Undergoing Primary Percutaneuos Coronary Intervention. 更正：MicroRNA-208a：接受初级经皮冠状动脉介入治疗的 STEMI 患者无再流的良好诊断标志物和预测因子。

IF 2.4 3区医学

Journal of Cardiovascular Translational Research Pub Date : 2024-08-01 DOI: 10.1007/s12265-024-10486-x

Aboubakr Mohamed Salama, Wael Ali Khalil, Manar Al-Zaky, Somia Hassan Abdallah, Nader Talaat Kandil, Ahmed Abdelsabour, Ahmed Mohammed Shaker, Mesbah Taha Hasanein, Giovanni Battista Luciani, Hassan M E Azzazy

引用次数: 0