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Cell Calcium. 2018 Jan;69:62-72. doi: 10.1016/j.ceca.2017.05.003. Epub 2017 May 5.

Mitochondrial and endoplasmic reticulum calcium homeostasis and cell death.

Author information

1
Dept. of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.
2
Dept. of Biochemistry, Nencki Institute of Experimental Biology, Warsaw, Poland.
3
Dept. of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy. Electronic address: paolo.pinton@unife.it.

Abstract

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.

KEYWORDS:

Apoptosis; Ca(2+) transfer; Calcium; Cell death; ER-mitochondria contact sites; Endoplasmic reticulum; Mitochondria; Mitochondria associated membranes (MAMs; Oncogenes; ROS; Tumor suppressors

PMID:
28515000
DOI:
10.1016/j.ceca.2017.05.003
[Indexed for MEDLINE]

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