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线粒体(功能)障碍与线粒体丰度之间的串扰。

Crosstalk between mitochondrial (dys)function and mitochondrial abundance.

机构信息

Laboratory of Biochemistry and Cell Biology (URBC), NARILIS (Namur Research Institute for Life Sciences), University of Namur (FUNDP), Namur, Belgium.

出版信息

J Cell Physiol. 2012 Jun;227(6):2297-310. doi: 10.1002/jcp.23021.

Abstract

A controlled regulation of mitochondrial mass through either the production (biogenesis) or the degradation (mitochondrial quality control) of the organelle represents a crucial step for proper mitochondrial and cell function. Key steps of mitochondrial biogenesis and quality control are overviewed, with an emphasis on the role of mitochondrial chaperones and proteases that keep mitochondria fully functional, provided the mitochondrial activity impairment is not excessive. In this case, the whole organelle is degraded by mitochondrial autophagy or "mitophagy." Beside the maintenance of adequate mitochondrial abundance and functions for cell homeostasis, mitochondrial biogenesis might be enhanced, through discussed signaling pathways, in response to various physiological stimuli, like contractile activity, exposure to low temperatures, caloric restriction, and stem cells differentiation. In addition, mitochondrial dysfunction might also initiate a retrograde response, enabling cell adaptation through increased mitochondrial biogenesis.

摘要

通过细胞器的产生(生物发生)或降解(线粒体质量控制)来控制线粒体质量的调节是线粒体和细胞功能正常的关键步骤。本文概述了线粒体生物发生和质量控制的关键步骤,并强调了线粒体伴侣蛋白和蛋白酶的作用,它们可以保持线粒体的正常功能,前提是线粒体的活性损伤不过度。在这种情况下,整个细胞器会被线粒体自噬或“自噬”降解。除了维持细胞内环境稳定所需的适当线粒体丰度和功能外,线粒体生物发生还可以通过讨论的信号通路增强,以响应各种生理刺激,如收缩活动、低温暴露、热量限制和干细胞分化。此外,线粒体功能障碍也可能引发逆行反应,通过增加线粒体生物发生使细胞适应。

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