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Immunometabolic switch in hypertension: how dendritic cell mineralocorticoid receptors drive Th17 polarization and blood pressure control.
IF 37.6 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-22 DOI: 10.1093/eurheartj/ehae863
Tomasz P Mikolajczyk, Tomasz Śliwa, Tomasz J Guzik
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引用次数: 0
Non-neuronal ventricular cardiomyocyte-located nicotinergic acetylcholine receptors cause remodelling and arrhythmias.
IF 37.6 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-22 DOI: 10.1093/eurheartj/ehae845
Sami F Noujaim, Dobromir Dobrev
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引用次数: 0
Weekly Journal Scan: Have we reached the SUMMIT of incretin treatment of heart failure with preserved ejection fraction and obesity? 每周杂志扫描:我们是否已经达到了肠促胰岛素治疗保留射血分数和肥胖的心力衰竭的顶峰?
IF 39.3 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1093/eurheartj/ehaf013
Giovanna Liuzzo,Carlo Patrono
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引用次数: 0
A Manifesto from Global Heart Hub for early detection and diagnosis of cardiovascular disease. 全球心脏中心关于早期检测和诊断心血管疾病的宣言。
IF 37.6 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1093/eurheartj/ehae455
Fausto J Pinto, Ed Harding, Olive Fenton
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引用次数: 0
Hypertrophic cardiomyopathy evolving management: American Heart Association/American College of Cardiology vs. European Society of Cardiology guidelines. 肥厚型心肌病的演变管理:美国心脏协会/美国心脏病学会与欧洲心脏病学会指南对比。
IF 37.6 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1093/eurheartj/ehae507
Edoardo Bertero, Marco Canepa, Iacopo Olivotto
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引用次数: 0
Weekly Journal Scan: RESHAPing potential treatment indications for functional mitral regurgitation in heart failure. 每周期刊扫描:RESHAPing 心力衰竭功能性二尖瓣反流的潜在治疗适应症。
IF 37.6 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1093/eurheartj/ehae727
Daniela Pedicino, Rocco Vergallo
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引用次数: 0
Targeting mitochondrial fitness for cardioprotection. 针对线粒体健康的心脏保护。
IF 37.6 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1093/eurheartj/ehae821
Sauri Hernandez-Resendiz, Derek J Hausenloy
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引用次数: 0
Desmoplakin cardiomyopathy: a step towards understanding the genetic basis of phenotypic and outcome heterogeneity. 桥状血小板性心肌病:迈向理解表型和结果异质性遗传基础的一步。
IF 37.6 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1093/eurheartj/ehae714
Adalena Tsatsopoulou, Soledad García-Hernández, William J McKenna
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引用次数: 0
Genetic testing in cardiomyopathies and new therapeutic target in cardiac remodelling. 心肌病基因检测与心脏重构治疗新靶点。
IF 39.3 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1093/eurheartj/ehae890
Filippo Crea
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引用次数: 0
Enhanced Parkin-mediated mitophagy mitigates adverse left ventricular remodelling after myocardial infarction: role of PR-364. 增强帕金介导的有丝分裂可减轻心肌梗死后左心室重塑的不利影响:PR-364 的作用。
IF 37.6 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2025-01-21 DOI: 10.1093/eurheartj/ehae782
Lizhuo Ai, Juliana de Freitas Germano, Chengqun Huang, Marianne Aniag, Savannah Sawaged, Jon Sin, Reetu Thakur, Deepika Rai, Christopher Rainville, David E Sterner, Yang Song, Honit Piplani, Suresh Kumar, Tauseef R Butt, Robert M Mentzer, Aleksandr Stotland, Roberta A Gottlieb, Jennifer E Van Eyk

Background and aims: Almost 30% of survivors of myocardial infarction (MI) develop heart failure (HF), in part due to damage caused by the accumulation of dysfunctional mitochondria. Organelle quality control through Parkin-mediated mitochondrial autophagy (mitophagy) is known to play a role in mediating protection against HF damage post-ischaemic injury and remodelling of the subsequent deteriorated myocardium.

Methods: This study has shown that a single i.p. dose (2 h post-MI) of the selective small molecule Parkin activator PR-364 reduced mortality, preserved cardiac ejection fraction, and mitigated the progression of HF. To reveal the mechanism of PR-364, a multi-omic strategy was deployed in combination with classical functional assays using in vivo MI and in vitro cardiomyocyte models.

Results: In vitro cell data indicated that Parkin activation by PR-364 increased mitophagy and mitochondrial biogenesis, enhanced adenosine triphosphate production via improved citric acid cycle, altered accumulation of calcium localization to the mitochondria, and initiated translational reprogramming with increased expression of mitochondrial translational proteins. In mice, PR-364 administered post-MI resulted in widespread proteome changes, indicating an up-regulation of mitochondrial metabolism and mitochondrial translation in the surviving myocardium.

Conclusions: This study demonstrates the therapeutic potential of targeting Parkin-mediated mitophagy using PR-364 to protect surviving cardiac tissue post-MI from progression to HF.

背景和目的:近30%的心肌梗死(MI)幸存者会出现心力衰竭(HF),部分原因是功能障碍线粒体的积累造成的损害。众所周知,通过帕金介导的线粒体自噬(mitophagy)进行细胞器质量控制,可在缺血损伤和随后恶化的心肌重塑中发挥作用,防止心力衰竭损伤:该研究表明,选择性小分子帕金激活剂 PR-364 的单次静脉注射剂量(心肌梗死后 2 小时)可降低死亡率、保护心脏射血分数并缓解高房颤动的进展。为了揭示 PR-364 的作用机制,我们采用了多组学策略,并结合使用体内心肌梗死和体外心肌细胞模型进行的经典功能测试:体外细胞数据表明,PR-364 对 Parkin 的激活增加了有丝分裂吞噬和线粒体生物生成,通过改善柠檬酸循环提高了三磷酸腺苷的产生,改变了线粒体的钙定位积累,并通过增加线粒体翻译蛋白的表达启动了翻译重编程。在小鼠中,心肌梗死后给药 PR-364 会导致广泛的蛋白质组变化,这表明存活心肌中的线粒体代谢和线粒体翻译得到了上调:本研究证明了利用 PR-364 靶向 Parkin 介导的有丝分裂的治疗潜力,以保护心肌梗死后存活的心脏组织,防止其发展为高房颤动。
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引用次数: 0
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European Heart Journal
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