How the disruption of mitochondrial redox signalling contributes to ageing

Castejon-Vega, B. , Cordero, M. D. and Sanz, A. (2023) How the disruption of mitochondrial redox signalling contributes to ageing. Antioxidants, 12(4), 831. (doi: 10.3390/antiox12040831) (PMID:37107206) (PMCID:PMC10135186)

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Abstract

In the past, mitochondrial reactive oxygen species (mtROS) were considered a byproduct of cellular metabolism. Due to the capacity of mtROS to cause oxidative damage, they were proposed as the main drivers of ageing and age-related diseases. Today, we know that mtROS are cellular messengers instrumental in maintaining cellular homeostasis. As cellular messengers, they are produced in specific places at specific times, and the intensity and duration of the ROS signal determine the downstream effects of mitochondrial redox signalling. We do not know yet all the processes for which mtROS are important, but we have learnt that they are essential in decisions that affect cellular differentiation, proliferation and survival. On top of causing damage due to their capacity to oxidize cellular components, mtROS contribute to the onset of degenerative diseases when redox signalling becomes dysregulated. Here, we review the best-characterized signalling pathways in which mtROS participate and those pathological processes in which they are involved. We focus on how mtROS signalling is altered during ageing and discuss whether the accumulation of damaged mitochondria without signalling capacity is a cause or a consequence of ageing.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Sanz Montero, Professor Alberto and Castejon Vega, Dr Beatriz
Authors: Castejon-Vega, B., Cordero, M. D., and Sanz, A.
College/School:College of Medical Veterinary and Life Sciences > School of Molecular Biosciences
Journal Name:Antioxidants
Publisher:MDPI
ISSN:2076-3921
ISSN (Online):2076-3921
Published Online:29 March 2023
Copyright Holders:Copyright © 2023 The Authors
First Published:First published in Antioxidants 12(4): 831
Publisher Policy:Reproduced under a Creative Commons License

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Project CodeAward NoProject NamePrincipal InvestigatorFunder's NameFunder RefLead Dept
310196Senior Research Fellowship, `ROS via RET: a redox regulated pathway to extend lifespanAlberto Sanz MonteroWellcome Trust (WELLCOTR)212241/A/18/ZInstitute of Molecular, Cell & Systems Biology
314830Why do mitochondria produce more ROS when we age?Alberto Sanz MonteroBiotechnology and Biological Sciences Research Council (BBSRC)BB/W006774/1Institute of Molecular, Cell & Systems Biology
313902Mitochondrial proteostasis and reductive metabolic stress in ageingKonstantinos TokatlidisBiotechnology and Biological Sciences Research Council (BBSRC)BB/W002892/1Institute of Molecular, Cell & Systems Biology
311154Rate of AutophagyAlberto Sanz MonteroBiotechnology and Biological Sciences Research Council (BBSRC)BB/R008167/2Institute of Molecular, Cell & Systems Biology