Death sentence: The tale of a fallen endoplasmic reticulum

Eoghan P McGrath; Federica G Centonze; Eric Chevet; Tony Avril; Elodie Lafont

doi:10.1016/j.bbamcr.2021.119001

Death sentence: The tale of a fallen endoplasmic reticulum

Biochim Biophys Acta Mol Cell Res. 2021 May;1868(6):119001. doi: 10.1016/j.bbamcr.2021.119001. Epub 2021 Mar 9.

Authors

Eoghan P McGrath¹, Federica G Centonze¹, Eric Chevet², Tony Avril², Elodie Lafont³

Affiliations

¹ Inserm U1242, University of Rennes, Rennes, France.
² Inserm U1242, University of Rennes, Rennes, France; Centre de Lutte Contre le Cancer Eugène Marquis, Rennes, France.
³ Inserm U1242, University of Rennes, Rennes, France. Electronic address: elodie.lafont@inserm.fr.

PMID: 33705817
DOI: 10.1016/j.bbamcr.2021.119001

Abstract

Endoplasmic Reticulum (ER) stress signaling is an adaptive mechanism triggered when protein folding demand overcomes the folding capacity of this compartment, thereby leading to the accumulation of improperly folded proteins. This stress signaling pathway is named the Unfolded Protein Response (UPR) and aims at restoring ER homeostasis. However, if this fails, mechanisms orienting cells towards death processes are initiated. Herein, we summarize the most recent findings connecting ER stress and the UPR with identified death mechanisms including apoptosis, necrosis, pyroptosis, ferroptosis, and autophagy. We highlight new avenues that could be investigated and controlled through actionable mechanisms in physiology and pathology.

Keywords: Apoptosis; Autophagy; Cell death; Endoplasmic reticulum; Ferroptosis; Pyroptosis; Unfolded protein response.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Apoptosis
Autophagy
Endoplasmic Reticulum / metabolism*
Endoplasmic Reticulum Stress*
Ferroptosis
Gene Expression Regulation
Humans
Unfolded Protein Response*