Mitochondrial and endoplasmic reticulum calcium homeostasis and cell death

被引:473
|
作者
Marchi, Saverio [1 ]
Patergnani, Simone [1 ]
Missiroli, Sonia [1 ]
Morciano, Giampaolo [1 ]
Rimessi, Alessandro [1 ]
Wieckowski, Mariusz R. [2 ]
Giorgi, Carlotta [1 ]
Pinton, Paolo [1 ]
机构
[1] Univ Ferrara, Dept Morphol Surg & Expt Med, Sect Pathol Oncol & Expt Biol, LTTA, Ferrara, Italy
[2] Nencki Inst Expt Biol, Dept Biochem, Warsaw, Poland
关键词
Endoplasmic reticulum; Mitochondria; Mitochondria associated membranes (MAMs); Calcium; ROS; ER-mitochondria contact sites; Ca2+ transfer; Cell death; Apoptosis; Oncogenes; Tumor suppressors; PERMEABILITY TRANSITION PORE; APOPTOTIC CA2+ SIGNALS; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTORS; CANCER-CELLS; IP3; RECEPTOR; MITOFUSIN; BH4; DOMAIN; ER STRESS; MOLECULAR-MECHANISMS; UNIPORTER COMPLEX;
D O I
10.1016/j.ceca.2017.05.003
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The endoplasmic reticulum (ER) and mitochondria cannot be considered as static structures, as they intimately communicate, forming very dynamic platforms termed mitochondria-associated membranes (MAMs). In particular, the ER transmits proper Ca2+ signals to mitochondria, which decode them into specific inputs to regulate essential functions, including metabolism, energy production and apoptosis. Here, we will describe the different molecular players involved in the transfer of Ca2+ ions from the ER lumen to the mitochondrial matrix and how modifications in both ER-mitochondria contact sites and Ca2+ signaling can alter the cell death execution program. (C) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:62 / 72
页数:11
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