Chronic heart failure following hemorrhagic myocardial infarction: mechanism, treatment and outlook.

IF 4.1 Q2 CELL BIOLOGY

Cell Stress Pub Date : 2023-02-01 DOI:10.15698/cst2023.02.276

Shing Fai Chan, Keyur Vora, Rohan Dharmakumar

引用次数: 1

Abstract

Myocardial infarction (MI), the blockage of arterial blood supply of the heart, is among the most common causes of death worldwide. Even when patients receive immediate treatment by re-opening blocked arteries, they often develop chronic heart failure (CHF) in the aftermath of MI events. Yet, the factors that contribute to the development of MI-associated CHF are poorly understood. In our recent study (Nat Commun 13:6394), we link intramyocardial hemorrhage, an injury which can occur during reperfusion of areas affected by MI, to an increased risk of CHF. Mechanistically, our data suggest that an iron-induced adverse cascade of events after hemorrhagic MI drives fatty degeneration of infarcted tissue, which ultimately contributes to negative cardiac remodeling. In this Microreview, we discuss the implications of our findings regarding the molecular mechanism, more targeted treatment options as well as perspectives in the clinical care of CHF after hemorrhagic MI.

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出血性心肌梗死后慢性心力衰竭:机制、治疗和前景。

心肌梗死(MI)，即心脏动脉血液供应的阻塞，是全世界最常见的死亡原因之一。即使患者立即接受重新打开阻塞动脉的治疗，他们也经常在心肌梗死事件后发生慢性心力衰竭(CHF)。然而，导致心肌梗死相关CHF发生的因素尚不清楚。在我们最近的研究中(Nat comm 13:63 . 94)，我们将心肌内出血(心肌梗死影响区域再灌注期间可能发生的损伤)与CHF风险增加联系起来。在机制上，我们的数据表明出血性心肌梗死后铁诱导的不良级联事件驱动梗死组织的脂肪变性，最终导致负性心脏重塑。在这篇微综述中，我们讨论了我们的研究结果在出血性心肌梗死后CHF的分子机制、更有针对性的治疗方案以及临床护理方面的意义。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Stress Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (miscellaneous)

CiteScore

13.50

自引率

0.00%

发文量

审稿时长

15 weeks

期刊介绍： Cell Stress is an open-access, peer-reviewed journal that is dedicated to publishing highly relevant research in the field of cellular pathology. The journal focuses on advancing our understanding of the molecular, mechanistic, phenotypic, and other critical aspects that underpin cellular dysfunction and disease. It specifically aims to foster cell biology research that is applicable to a range of significant human diseases, including neurodegenerative disorders, myopathies, mitochondriopathies, infectious diseases, cancer, and pathological aging. The scope of Cell Stress is broad, welcoming submissions that represent a spectrum of research from fundamental to translational and clinical studies. The journal is a valuable resource for scientists, educators, and policymakers worldwide, as well as for any individual with an interest in cellular pathology. It serves as a platform for the dissemination of research findings that are instrumental in the investigation, classification, diagnosis, and therapeutic management of major diseases. By being open-access, Cell Stress ensures that its content is freely available to a global audience, thereby promoting international scientific collaboration and accelerating the exchange of knowledge within the research community.