线粒体钙信号和神经退行性疾病。

Q4 Neuroscience Neuronal signaling Pub Date : 2018-11-16 eCollection Date: 2018-12-01 DOI:10.1042/NS20180061
Elena Britti, Fabien Delaspre, Jordi Tamarit, Joaquim Ros
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引用次数: 33

摘要

钙被细胞用于信号传导和调节ATP的产生;它还有助于细胞存活,当浓度不平衡时,触发细胞死亡的途径。线粒体有助于钙缓冲,这意味着线粒体钙的摄取和释放与细胞质钙浓度密切相关。本文综述了有助于线粒体钙稳态的蛋白质,线粒体通透性过渡孔(MPTP)和线粒体钙活化蛋白的作用,以及它们在神经退行性病理中的相关性。它还涵盖了弗里德赖希共济失调(FA)中钙稳态的改变。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Mitochondrial calcium signalling and neurodegenerative diseases.

Calcium is utilised by cells in signalling and in regulating ATP production; it also contributes to cell survival and, when concentrations are unbalanced, triggers pathways for cell death. Mitochondria contribute to calcium buffering, meaning that mitochondrial calcium uptake and release is intimately related to cytosolic calcium concentrations. This review focuses on the proteins contributing to mitochondrial calcium homoeostasis, the roles of the mitochondrial permeability transition pore (MPTP) and mitochondrial calcium-activated proteins, and their relevance in neurodegenerative pathologies. It also covers alterations to calcium homoeostasis in Friedreich ataxia (FA).

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来源期刊
CiteScore
4.60
自引率
0.00%
发文量
0
审稿时长
14 weeks
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