Apoptotic signals at the endoplasmic reticulum-mitochondria interface

被引:21
|
作者
Giamogante, Flavia [1 ]
Poggio, Elena [1 ]
Barazzuol, Lucia [1 ]
Covallero, Alberto [1 ]
Cali, Tito [1 ]
机构
[1] Univ Padua, Dept Biomed Sci, Padua, Italy
来源
关键词
INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; CELL-DEATH; ER-STRESS; CALCIUM UNIPORTER; CA2+ RELEASE; MITOFUSIN; REGULATES APOPTOSIS; MEMBRANE-FRACTION; DISTINCT ROLES; OUTER-MEMBRANE;
D O I
10.1016/bs.apcsb.2021.02.007
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The maintenance of cellular homeostasis involves the participation of multiple organelles, such as the endoplasmic reticulum (ER) and mitochondria. Specifically, ER plays a key role in calcium (Ca2+) storage, lipid synthesis, protein folding, and assembly, while mitochondria are the "energy factories" and provide energy to drive intracellular processes. Hence, alteration in ER or mitochondrial homeostasis has detrimental effects on cell survival, being linked to the triggering of apoptosis, a programmed form of cell death. Besides, ER stress conditions affect mitochondria functionality and vice-versa, as ER and mitochondria communicate via mitochondria-associated ER membranes (MAMs) to carry out a number of fundamental cellular functions. It is not surprising, thus, that also MAMs perturbations are involved in the regulation of apoptosis. This chapter intends to accurately discuss the involvement of MAMs in apoptosis, highlighting their crucial role in controlling this delicate cellular process.
引用
收藏
页码:307 / 343
页数:37
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