Intracellular Ca2+ signaling and Ca2+ microdomains in the control of cell survival, apoptosis and autophagy

被引:215
|
作者
La Rovere, Rita M. L.
Roest, Gemma
Bultynck, Geert [1 ]
Parys, Jan B. [1 ]
机构
[1] Katholieke Univ Leuven, Lab Mol & Cellular Signaling, Dept Cellular & Mol Med, Campus Gasthuisberg O-N-1 B-802, BE-3000 Leuven, Belgium
关键词
Apoptosis; Autophagy; Endoplasmic reticulum; IP3; receptor; Lysosomes; Mitochondria; MITOCHONDRIAL CALCIUM UNIPORTER; PERMEABILITY TRANSITION PORE; DEPENDENT ANION CHANNEL; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; ADENINE-DINUCLEOTIDE PHOSPHATE; ENDOPLASMIC-RETICULUM ER; BCL-2; FAMILY-MEMBERS; VDAC1; N-TERMINUS; RYANODINE RECEPTOR; BH4; DOMAIN;
D O I
10.1016/j.ceca.2016.04.005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The endoplasmic reticulum (ER), mitochondria and lysosomes are physically and/or functionally linked, establishing close contact sites between these organelles. As a consequence, Ca2+ release events from the ER, the major intracellular Ca2+-storage organelle, have an immediate effect on the physiological function of mitochondria and lysosomes. Also, the lysosomes can act as a Ca2+ source for Ca2+ release into the cytosol, thereby influencing ER-based Ca2+ signaling. Given the important role for mitochondria and lysosomes in cell survival, cell death and cell adaptation processes, it has become increasingly clear that Ca2+ signals from or towards these organelles impact these processes. In this review, we discuss the most recent insights in the emerging role of Ca2+ signaling in cellular survival by controlling basal mitochondrial bioenergetics and by regulating apoptosis, a mitochondrial process, and autophagy, a lysosomal process, in response to cell damage and cell stress. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:74 / 87
页数:14
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