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心肌梗死是线粒体功能障碍的后果。

Myocardial Infarction as a Consequence of Mitochondrial Dysfunction.

机构信息

PSIT-Pranveer Singh Institute of Technology (Pharmacy), Bhauti, Kanpur, UP-209305, India.

Department of Pharmacy Practice, NIMS Institute of Pharmacy, NIMS University, Jaipur, Rajasthan, India.

出版信息

Curr Cardiol Rev. 2023;19(6):23-30. doi: 10.2174/1573403X19666230508114311.

Abstract

Acute myocardial infarction is an event of myocardial necrosis caused by unstable ischemic syndrome. Myocardial infarction (MI) occurs when blood stops flowing to the cardiac tissue or myocardium and the heart muscle gets damaged due to poor perfusion and reduced oxygen supply. Mitochondria can serve as the arbiter of cell fate in response to stress. Oxidative metabolism is the function of mitochondria within the cell. Cardiac cells being highly oxidative tissue generates about 90% of their energy through oxidative metabolism. In this review, we focused on the role of mitochondria in energy generation in myocytes as well as its consequences on heart cells causing cell damage. The role of mitochondrial dysfunction due to oxidative stress, production of reactive oxygen species, and anaerobic production of lactate as a failure of oxidative metabolism are also discussed.

摘要

急性心肌梗死是由不稳定型缺血综合征引起的心肌坏死事件。心肌梗死(MI)发生于血流中断导致心肌组织或心肌受损,进而使心脏灌注不良和供氧减少时。线粒体可作为细胞应激反应中命运的裁决者。氧化代谢是细胞内线粒体的功能。心脏细胞是高度氧化组织,约 90%的能量通过氧化代谢产生。在这篇综述中,我们重点关注线粒体在心肌细胞能量生成中的作用及其对导致心肌细胞损伤的细胞损伤的后果。还讨论了氧化应激、活性氧产生和无氧乳酸生成导致氧化代谢失败引起的线粒体功能障碍的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/16fa/10636795/9fd9b8130e50/CCR-19-E080523216642_F1.jpg

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