IP(3) Receptors, Mitochondria, and Ca Signaling: Implications for Aging.
IP(3) Receptors, Mitochondria, and Ca Signaling: Implications for Aging.
复制标题
DOI：
10.4061/2011/920178
复制
发表时间：
2011-03-08
影响因子：
4.7
通讯作者：
Bultynck G
中科院分区：
文献类型：
--
作者：
Decuypere JP;Monaco G;Missiaen L;De Smedt H;Parys JB;Bultynck G
内质网-（ER-）和Ca 2 +-介导的Ca 2+信号传导之间的紧密相互作用是通过控制细胞凋亡和自噬的细胞健康和细胞命运的关键决定因素。阻止或促进细胞凋亡和自噬的蛋白质可以通过结合和调节细胞内Ca 2+释放和Ca 2+摄取机制来影响细胞内Ca 2+动力学和稳态。在衰老过程中，氧化应激成为影响ER和线粒体功能的额外因素，从而影响它们在Ca 2+信号传导中的作用。重要的是，线粒体功能障碍和持续的线粒体损伤可能是衰老过程的一部分。在本文中，我们将讨论不同的机制，控制细胞内Ca 2+信号与细胞凋亡和自噬，并审查这些过程是如何影响衰老过程中通过积累活性氧。
The tight interplay between endoplasmic-reticulum-(ER-) and mitochondria-mediated Ca2+ signaling is a key determinant of cellular health and cellular fate through the control of apoptosis and autophagy. Proteins that prevent or promote apoptosis and autophagy can affect intracellular Ca2+ dynamics and homeostasis through binding and modulation of the intracellular Ca2+-release and Ca2+-uptake mechanisms. During aging, oxidative stress becomes an additional factor that affects ER and mitochondrial function and thus their role in Ca2+ signaling. Importantly, mitochondrial dysfunction and sustained mitochondrial damage are likely to underlie part of the aging process. In this paper, we will discuss the different mechanisms that control intracellular Ca2+ signaling with respect to apoptosis and autophagy and review how these processes are affected during aging through accumulation of reactive oxygen species.