铁代谢及铁死亡在心肌病中的作用及调控机制研究进展
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R542.2,R363.2+1

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国家自然科学基金重点项目(81730057;82130062);河北省医学科学研究课题(20210013)


Update on the potential role and its regulatory mechanism of iron metabolism and ferroptosis of cardiomyocytes in cardiomyopathy
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    摘要:

    心肌细胞代谢及死亡方式是心肌病的重要病理生理学基础。许多研究提示,铁代谢紊乱是心肌病发生发展的关键环节之一。铁是人体重要生理功能所必需的矿物质,参与细胞呼吸、脂质代谢以及蛋白质合成;在病理条件下,铁蓄积诱导的毒性作用可破坏心肌细胞稳态和活力,导致细胞死亡,即铁死亡。过量的铁则通过芬顿反应诱导过氧化物生成,造成心肌细胞功能损害。因此,铁死亡在调控心肌病的发生及发展过程中具有重要意义。本文总结了铁代谢及铁死亡在心肌病中的病理生理改变及其调控机制,深刻认识铁代谢及铁死亡的调控靶点将为心肌病防治开辟新途径。

    Abstract:

    It has been demonstrated that cardiomyocyte metabolism and cell death are the fundamental progresses in the development of cardiomyopathy. Increasing evidences suggest that metabolic imbalance of iron appears to be involved in the pathophysiology of cardiomyopathy. As we well known, iron is an essential mineral required for various functions, including cellular respiration, lipid and oxygen metabolism, as well as protein synthesis. However, cardiomyocyte homeostasis and viability are inclined to be jeopardized by iron-induced toxicity under pathological stress, which is defined as ferroptosis. In the pathogenesis of cardiomyopathy, excessive iron is transported into cells that drives cardiomyocytes more vulnerable to ferroptosis by the accumulation of reactive oxygen species through Fenton reaction. The enhanced induction of reactive oxygen species in ferroptosis leads cardiomyocytes to become more sensitive to oxidative stress under the exposure of excess iron. Thus, ferroptosis might play an important role in the pathogenic progression of cardiomyopathy, and precisely targeting ferroptosis mechanisms may be a promising therapeutic option to revert myocardialremodeling. This review summarizes the pathophysiological alterations from iron homeostasis to ferroptosis together with signaling transduction with regard to ferroptosis in cardiomyopathy.

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  • 在线发布日期: 2022-01-14
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