Molecular Signaling to Preserve Mitochondrial Integrity against Ischemic Stress in the Heart: Rescue or Remove Mitochondria in Danger.

Molecular Signaling to Preserve Mitochondrial Integrity against Ischemic Stress in the Heart: Rescue or Remove Mitochondria in Danger.
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保护线粒体完整性对抗心脏缺血应激的分子信号:挽救或清除危险中的线粒体。

DOI:
10.3390/cells10123330
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发表时间:
2021-11-27
期刊:
影响因子:
6
通讯作者:
Miyamoto S
Miyamoto S
中科院分区:
生物学2区
文献类型:
--
作者:
Yu JD;Miyamoto S

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心血管疾病是世界范围内导致死亡和全球健康问题的主要原因之一,而缺血性心脏病是心力衰竭(HF)最常见的原因。心脏是一个能量要求很高的器官,而心肌的能量储备是有限的。线粒体是细胞的动力源,但在应激条件下,它们会受到破坏,释放坏死和凋亡因子,并导致细胞死亡。心肌细胞丢失在缺血性心脏病中起着重要作用。作为对压力的反应,保护性信号通路被激活以限制线粒体的退化并保护心脏。为了防止线粒体死亡途径,受损的线粒体通过线粒体自噬(有丝分裂)被移除。线粒体吞噬作用介导的线粒体质量控制在功能上与线粒体动力学有关。这篇综述提供了对线粒体完整性在心脏中抵抗缺血应激保护的信号机制的最新理解。
Cardiovascular diseases are one of the leading causes of death and global health problems worldwide, and ischemic heart disease is the most common cause of heart failure (HF). The heart is a high-energy demanding organ, and myocardial energy reserves are limited. Mitochondria are the powerhouses of the cell, but under stress conditions, they become damaged, release necrotic and apoptotic factors, and contribute to cell death. Loss of cardiomyocytes plays a significant role in ischemic heart disease. In response to stress, protective signaling pathways are activated to limit mitochondrial deterioration and protect the heart. To prevent mitochondrial death pathways, damaged mitochondria are removed by mitochondrial autophagy (mitophagy). Mitochondrial quality control mediated by mitophagy is functionally linked to mitochondrial dynamics. This review provides a current understanding of the signaling mechanisms by which the integrity of mitochondria is preserved in the heart against ischemic stress.
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