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线粒体控制对缺氧的急性和慢性反应。

Mitochondria control acute and chronic responses to hypoxia.

作者信息

McElroy G S, Chandel N S

机构信息

Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, United States.

Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, United States.

出版信息

Exp Cell Res. 2017 Jul 15;356(2):217-222. doi: 10.1016/j.yexcr.2017.03.034. Epub 2017 Mar 19.

DOI:10.1016/j.yexcr.2017.03.034
PMID:28327410
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5474758/
Abstract

There are numerous mechanisms by which mammals respond to hypoxia. These include acute changes in pulmonary arterial tone due to smooth muscle cell contraction, acute increases in respiration triggered by the carotid body chemosensory cells, and chronic changes such as induction of red blood cell proliferation and angiogenesis by hypoxia inducible factor targets erythropoietin and vascular endothelial growth factor, respectively. Mitochondria account for the majority of oxygen consumption in the cell and have recently been appreciated to serve as signaling organelles required for the initiation or propagation of numerous homeostatic mechanisms. Mitochondria can influence cell signaling by production of reactive oxygen species and metabolites. Here we review recent evidence that mitochondrial signals can imitate acute and chronic hypoxia responses.

摘要

哺乳动物对缺氧作出反应的机制众多。这些机制包括因平滑肌细胞收缩导致的肺动脉张力急性变化、由颈动脉体化学感应细胞触发的呼吸急性增加,以及慢性变化,如分别通过缺氧诱导因子的靶标促红细胞生成素和血管内皮生长因子诱导红细胞增殖和血管生成。线粒体消耗细胞内大部分氧气,最近人们认识到它作为启动或传播众多稳态机制所需的信号细胞器。线粒体可通过产生活性氧和代谢产物来影响细胞信号传导。在此,我们综述了线粒体信号可模拟急性和慢性缺氧反应的最新证据。

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