Toggle Main Menu Toggle Search

Open Access padlockePrints

The evolution of selective autophagy as a mechanism of oxidative stress response: The evolutionarily acquired ability of selective autophagy receptors to respond to oxidative stress is beneficial for human longevity

Lookup NU author(s): Joshua Ratliffe, Dr Tetsushi Kataura, Gisela Otten, Professor Viktor KorolchukORCiD

Downloads


Licence

This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).


Abstract

© 2023 The Authors. BioEssays published by Wiley Periodicals LLC. Ageing is associated with a decline in autophagy and elevated reactive oxygen species (ROS), which can breach the capacity of antioxidant systems. Resulting oxidative stress can cause further cellular damage, including DNA breaks and protein misfolding. This poses a challenge for longevous organisms, including humans. In this review, we hypothesise that in the course of human evolution selective autophagy receptors (SARs) acquired the ability to sense and respond to localised oxidative stress. We posit that in the vicinity of protein aggregates and dysfunctional mitochondria oxidation of key cysteine residues in SARs induces their oligomerisation which initiates autophagy. The degradation of damaged cellular components thus could reduce ROS production and restore redox homeostasis. This evolutionarily acquired function of SARs may represent one of the biological adaptations that contributed to longer lifespan. Inversely, loss of this mechanism can lead to age-related diseases associated with impaired autophagy and oxidative stress.


Publication metadata

Author(s): Ratliffe J, Kataura T, Otten EG, Korolchuk VI

Publication type: Review

Publication status: Published

Journal: BioEssays

Year: 2023

Volume: 45

Issue: 11

Print publication date: 01/11/2023

Online publication date: 21/08/2023

Acceptance date: 02/08/2023

ISSN (print): 0265-9247

ISSN (electronic): 1521-1878

Publisher: John Wiley and Sons Inc

URL: https://doi.org/10.1002/bies.202300076

DOI: 10.1002/bies.202300076

PubMed id: 37603398

Data Access Statement: Any information reported in this paper is available from the corresponding author (V.I.K.) upon request.


Share