Mitochondria and inflammation: cell death heats up

Vringer, E. and Tait, S. W.G. (2019) Mitochondria and inflammation: cell death heats up. Frontiers in Cell and Developmental Biology, 7, 100. (doi:10.3389/fcell.2019.00100)

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Abstract

Mitochondrial outer membrane permeabilization (MOMP) is essential to initiate mitochondrial apoptosis. Due to the disruption of mitochondrial outer membrane integrity, intermembrane space proteins, notably cytochrome c, are released into the cytosol whereupon they activate caspase proteases and apoptosis. Beyond its well-established apoptotic role, MOMP has recently been shown to display potent pro-inflammatory effects. These include mitochondrial DNA dependent activation of cGAS-STING signaling leading to a type I interferon response. Secondly, via an IAP-regulated mechanism, MOMP can engage pro-inflammatory NF-κB signaling. During cell death, apoptotic caspase activity inhibits mitochondrial dependent inflammation. Importantly, by engaging an immunogenic form of cell death, inhibiting caspase function can effectively inhibit tumorigenesis. Unexpectedly, these studies reveal mitochondria as inflammatory signaling hubs during cell death and demonstrate its potential for therapeutic exploitation.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Vringer, Esmee and Tait, Professor Stephen
Authors: Vringer, E., and Tait, S. W.G.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cancer Sciences
Journal Name:Frontiers in Cell and Developmental Biology
Publisher:Frontiers Media
ISSN:2296-634X
ISSN (Online):2296-634X
Copyright Holders:Copyright © 2019 Vringer and Tait
First Published:First published in Frontiers in Cell and Developmental Biology 7:100
Publisher Policy:Reproduced under a Creative Commons license

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