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活性氧、自噬和代谢在心肌缺血和再灌注阶段的相互作用。

Crosstalk among Reactive Oxygen Species, Autophagy and Metabolism in Myocardial Ischemia and Reperfusion Stages.

机构信息

Key Laboratory of Advanced Pharmaceutical Technology, Ministry of Education of China; School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, Henan, China.

Department of Pharmacology, School of Pharmaceutical Sciences, Fudan University, Shanghai, China.

出版信息

Aging Dis. 2024 May 7;15(3):1075-1107. doi: 10.14336/AD.2023.0823-4.

DOI:10.14336/AD.2023.0823-4
PMID:37728583
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11081167/
Abstract

Myocardial ischemia is the most common cardiovascular disease. Reperfusion, an important myocardial ischemia tool, causes unexpected and irreversible damage to cardiomyocytes, resulting in myocardial ischemia/reperfusion (MI/R) injury. Upon stress, especially oxidative stress induced by reactive oxygen species (ROS), autophagy, which degrades the intracellular energy storage to produce metabolites that are recycled into metabolic pathways to buffer metabolic stress, is initiated during myocardial ischemia and MI/R injury. Excellent cardioprotective effects of autophagy regulators against MI and MI/R have been reported. Reversing disordered cardiac metabolism induced by ROS also exhibits cardioprotective action in patients with myocardial ischemia. Herein, we review current knowledge on the crosstalk between ROS, cardiac autophagy, and metabolism in myocardial ischemia and MI/R. Finally, we discuss the possible regulators of autophagy and metabolism that can be exploited to harness the therapeutic potential of cardiac metabolism and autophagy in the diagnosis and treatment of myocardial ischemia and MI/R.

摘要

心肌缺血是最常见的心血管疾病。再灌注作为一种重要的心肌缺血治疗手段,会导致心肌细胞发生意外且不可逆转的损伤,进而引起心肌缺血/再灌注(MI/R)损伤。在应激状态下,特别是活性氧(ROS)诱导的氧化应激下,自噬会被启动,通过降解细胞内的能量储存来产生代谢物,这些代谢物被回收再利用到代谢途径中,以缓冲代谢应激。自噬调节剂在心肌缺血和 MI/R 损伤中具有出色的心脏保护作用。逆转 ROS 诱导的心脏代谢紊乱也在心肌缺血患者中表现出心脏保护作用。在此,我们综述了 ROS、心脏自噬和心肌缺血及 MI/R 中代谢之间相互作用的最新知识。最后,我们讨论了可能的自噬和代谢调节剂,这些调节剂可以被利用来挖掘心脏代谢和自噬在心肌缺血和 MI/R 的诊断和治疗中的治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/1d19aa0b9c48/AD-15-3-1075-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/7b25e64464fc/AD-15-3-1075-g1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/7080bb2315c5/AD-15-3-1075-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/52c65d6eddf2/AD-15-3-1075-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/1d19aa0b9c48/AD-15-3-1075-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/7b25e64464fc/AD-15-3-1075-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/995cc2ded68b/AD-15-3-1075-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/7080bb2315c5/AD-15-3-1075-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/52c65d6eddf2/AD-15-3-1075-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7667/11081167/1d19aa0b9c48/AD-15-3-1075-g5.jpg

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