自噬启动过程中的线粒体钙运输

Sujyoti Chandra, Parul Katiyar, Aarooran S. Durairaj, Xinnan Wang
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引用次数: 0

摘要

虽然研究表明,ER 膜上的 Ca2+ 动态对某些类型的自噬(如饥饿诱导的自噬)的启动至关重要,但线粒体 Ca2+ 转运在自噬第一阶段如何变化还没有系统的描述。对自噬启动过程中线粒体 Ca2+ 动态的研究可能有助于我们确定自噬与线粒体 Ca2+ 通量之间的关系。在这里,我们研究了不同类型细胞中线粒体和ER对一系列自噬诱导剂的急性钙反应。不同的自噬诱导剂会触发线粒体 Ca2+ 转运和 ER 膜上的 Ca2+ 瞬态。有丝分裂诱导剂引发的线粒体 Ca2+ 摄取依赖于线粒体钙离子单向传输器,可能会减缓随后的有丝分裂。在帕金森病人的神经元中,有丝分裂诱导剂触发的线粒体 Ca2+ 流入速度更快,这可能会减缓随后的有丝分裂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mitochondrial calcium transport during autophagy initiation

While it has been shown that Ca2+ dynamics at the ER membrane is essential for the initiation of certain types of autophagy such as starvation-induced autophagy, how mitochondrial Ca2+ transport changes during the first stage of autophagy is not systemically characterized. An investigation of mitochondrial Ca2+ dynamics during autophagy initiation may help us determine the relationship between autophagy and mitochondrial Ca2+ fluxes. Here we examine acute mitochondrial and ER calcium responses to a panel of autophagy inducers in different cell types. Mitochondrial Ca2+ transport and Ca2+ transients at the ER membrane are triggered by different autophagy inducers. The mitophagy-inducer-initiated mitochondrial Ca2+ uptake relies on mitochondrial calcium uniporter and may decelerate the following mitophagy. In neurons derived from a Parkinson's patient, mitophagy-inducer-triggered mitochondrial Ca2+ influx is faster, which may slow the ensuing mitophagy.

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