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线粒体释放的Ca(2+)的命运。

The destiny of Ca(2+) released by mitochondria.

作者信息

Takeuchi Ayako, Kim Bongju, Matsuoka Satoshi

机构信息

Department of Integrative and Systems Physiology, Faculty of Medical Sciences, University of Fukui, 23-3, Matsuokashimoaizuki, Eiheiji-cho, Yoshida-gun, Fukui, 910-1193, Japan,

出版信息

J Physiol Sci. 2015 Jan;65(1):11-24. doi: 10.1007/s12576-014-0326-7. Epub 2014 Jul 4.

DOI:10.1007/s12576-014-0326-7
PMID:24994533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4276810/
Abstract

Mitochondrial Ca(2+) is known to regulate diverse cellular functions, for example energy production and cell death, by modulating mitochondrial dehydrogenases, inducing production of reactive oxygen species, and opening mitochondrial permeability transition pores. In addition to the action of Ca(2+) within mitochondria, Ca(2+) released from mitochondria is also important in a variety of cellular functions. In the last 5 years, the molecules responsible for mitochondrial Ca(2+) dynamics have been identified: a mitochondrial Ca(2+) uniporter (MCU), a mitochondrial Na(+)-Ca(2+) exchanger (NCLX), and a candidate for a mitochondrial H(+)-Ca(2+) exchanger (Letm1). In this review, we focus on the mitochondrial Ca(2+) release system, and discuss its physiological and pathophysiological significance. Accumulating evidence suggests that the mitochondrial Ca(2+) release system is not only crucial in maintaining mitochondrial Ca(2+) homeostasis but also participates in the Ca(2+) crosstalk between mitochondria and the plasma membrane and between mitochondria and the endoplasmic/sarcoplasmic reticulum.

摘要

线粒体钙(Ca²⁺)通过调节线粒体脱氢酶、诱导活性氧生成以及开放线粒体通透性转换孔来调控多种细胞功能,如能量产生和细胞死亡。除了Ca²⁺在线粒体内的作用外,线粒体释放的Ca²⁺在多种细胞功能中也很重要。在过去5年里,已鉴定出负责线粒体Ca²⁺动态变化的分子:线粒体钙单向转运体(MCU)、线粒体钠钙交换体(NCLX)以及线粒体氢钙交换体的候选分子(Letm1)。在本综述中,我们聚焦于线粒体Ca²⁺释放系统,并讨论其生理和病理生理意义。越来越多的证据表明,线粒体Ca²⁺释放系统不仅在维持线粒体Ca²⁺稳态中至关重要,还参与线粒体与质膜之间以及线粒体与内质网/肌浆网之间的Ca²⁺信号交流。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/cb3cc1fac23d/12576_2014_326_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/5a64762c27b0/12576_2014_326_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/9f4d188ce676/12576_2014_326_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/483a2160fb38/12576_2014_326_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/8b4d911f336d/12576_2014_326_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/cb3cc1fac23d/12576_2014_326_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/5a64762c27b0/12576_2014_326_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/9f4d188ce676/12576_2014_326_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/483a2160fb38/12576_2014_326_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/8b4d911f336d/12576_2014_326_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/37d7/10717822/cb3cc1fac23d/12576_2014_326_Fig5_HTML.jpg

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