Citation

Borisenko GG. Lipid Technology 2016; 28(2): 40-43.

Copyright

(Copyright © 2016)

DOI

10.1002/lite.201600009

PMID

unavailable

Abstract

Cardiolipin is an important component of the phospholipids constituting the inner membranes in mitochondria, the powerhouses of human cells. The process of oxidative phosphorylation in mitochondria that produces adenosine triphosphate (ATP) molecules is also accompanied, particularly under oxidative stress, by the formation of reactive oxygen species (ROS). ROS may in turn lead to the damage of mitochondrial machinery and even to the death of the host cell. Here we describe the role of cardiolipin in the normally functioning mitochondria as well as its regulatory function as a trigger of either natural elimination of damaged mitochondria without the host cell inquiry (mitophagy) or a programmed host cell death (apoptosis). Special attention is paid to the redistribution of cardiolipin between the membranes of damaged mitochondria as an "eat-me" signal for mitophagy and the subsequent oxidation of this phospholipid catalyzed by its complex with electron transfer protein cytochrome c that leads finally to the cell suicide or apoptosis. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

Language: en

Keywords

Apoptosis; Mitochondria; Oxidative stress; Cells; Reactive oxygen species; Cell death; Phospholipids; Cytology; Machinery; Cytochrome c; Cardiolipin; Cardiolipins; Adenosinetriphosphate; Cytochrome C; Electron transfer proteins; Human cells; Inner membranes; Oxidative phosphorylation; Regulatory functions