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Mitochondrial autophagy in the sleeping brain

A significant percentage of the mitochondrial mass is replaced on a daily basis via mechanisms of mitochondrial quality control. Through mitophagy (a selective type of autophagy that promotes mitochondrial proteostasis) cells keep a healthy pool of mitochondria, and prevent oxidative stress and infl...

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Autores principales: Mauri, Sofia, Favaro, Mariavittoria, Bernardo, Greta, Mazzotta, Gabriella M., Ziviani, Elena
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9449320/
https://www.ncbi.nlm.nih.gov/pubmed/36092697
http://dx.doi.org/10.3389/fcell.2022.956394
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author Mauri, Sofia
Favaro, Mariavittoria
Bernardo, Greta
Mazzotta, Gabriella M.
Ziviani, Elena
author_facet Mauri, Sofia
Favaro, Mariavittoria
Bernardo, Greta
Mazzotta, Gabriella M.
Ziviani, Elena
author_sort Mauri, Sofia
collection PubMed
description A significant percentage of the mitochondrial mass is replaced on a daily basis via mechanisms of mitochondrial quality control. Through mitophagy (a selective type of autophagy that promotes mitochondrial proteostasis) cells keep a healthy pool of mitochondria, and prevent oxidative stress and inflammation. Furthermore, mitophagy helps adapting to the metabolic demand of the cells, which changes on a daily basis. Core components of the mitophagy process are PINK1 and Parkin, which mutations are linked to Parkinson’s Disease. The crucial role of PINK1/Parkin pathway during stress-induced mitophagy has been extensively studied in vitro in different cell types. However, recent advances in the field allowed discovering that mitophagy seems to be only slightly affected in PINK1 KO mice and flies, putting into question the physiological relevance of this pathway in vivo in the whole organism. Indeed, several cell-specific PINK1/Parkin-independent mitophagy pathways have been recently discovered, which appear to be activated under physiological conditions such as those that promote mitochondrial proteome remodeling during differentiation or in response to specific physiological stimuli. In this Mini Review we want to summarize the recent advances in the field, and add another level of complexity by focusing attention on a potentially important aspect of mitophagy regulation: the implication of the circadian clock. Recent works showed that the circadian clock controls many aspects of mitochondrial physiology, including mitochondrial morphology and dynamic, respiratory activity, and ATP synthesis. Furthermore, one of the essential functions of sleep, which is controlled by the clock, is the clearance of toxic metabolic compounds from the brain, including ROS, via mechanisms of proteostasis. Very little is known about a potential role of the clock in the quality control mechanisms that maintain the mitochondrial repertoire healthy during sleep/wake cycles. More importantly, it remains completely unexplored whether (dys)function of mitochondrial proteostasis feedbacks to the circadian clockwork.
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spelling pubmed-94493202022-09-08 Mitochondrial autophagy in the sleeping brain Mauri, Sofia Favaro, Mariavittoria Bernardo, Greta Mazzotta, Gabriella M. Ziviani, Elena Front Cell Dev Biol Cell and Developmental Biology A significant percentage of the mitochondrial mass is replaced on a daily basis via mechanisms of mitochondrial quality control. Through mitophagy (a selective type of autophagy that promotes mitochondrial proteostasis) cells keep a healthy pool of mitochondria, and prevent oxidative stress and inflammation. Furthermore, mitophagy helps adapting to the metabolic demand of the cells, which changes on a daily basis. Core components of the mitophagy process are PINK1 and Parkin, which mutations are linked to Parkinson’s Disease. The crucial role of PINK1/Parkin pathway during stress-induced mitophagy has been extensively studied in vitro in different cell types. However, recent advances in the field allowed discovering that mitophagy seems to be only slightly affected in PINK1 KO mice and flies, putting into question the physiological relevance of this pathway in vivo in the whole organism. Indeed, several cell-specific PINK1/Parkin-independent mitophagy pathways have been recently discovered, which appear to be activated under physiological conditions such as those that promote mitochondrial proteome remodeling during differentiation or in response to specific physiological stimuli. In this Mini Review we want to summarize the recent advances in the field, and add another level of complexity by focusing attention on a potentially important aspect of mitophagy regulation: the implication of the circadian clock. Recent works showed that the circadian clock controls many aspects of mitochondrial physiology, including mitochondrial morphology and dynamic, respiratory activity, and ATP synthesis. Furthermore, one of the essential functions of sleep, which is controlled by the clock, is the clearance of toxic metabolic compounds from the brain, including ROS, via mechanisms of proteostasis. Very little is known about a potential role of the clock in the quality control mechanisms that maintain the mitochondrial repertoire healthy during sleep/wake cycles. More importantly, it remains completely unexplored whether (dys)function of mitochondrial proteostasis feedbacks to the circadian clockwork. Frontiers Media S.A. 2022-08-24 /pmc/articles/PMC9449320/ /pubmed/36092697 http://dx.doi.org/10.3389/fcell.2022.956394 Text en Copyright © 2022 Mauri, Favaro, Bernardo, Mazzotta and Ziviani. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Mauri, Sofia
Favaro, Mariavittoria
Bernardo, Greta
Mazzotta, Gabriella M.
Ziviani, Elena
Mitochondrial autophagy in the sleeping brain
title Mitochondrial autophagy in the sleeping brain
title_full Mitochondrial autophagy in the sleeping brain
title_fullStr Mitochondrial autophagy in the sleeping brain
title_full_unstemmed Mitochondrial autophagy in the sleeping brain
title_short Mitochondrial autophagy in the sleeping brain
title_sort mitochondrial autophagy in the sleeping brain
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9449320/
https://www.ncbi.nlm.nih.gov/pubmed/36092697
http://dx.doi.org/10.3389/fcell.2022.956394
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