Cargando…
The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword?
Peroxisomes harbor numerous enzymes that can produce or degrade hydrogen peroxide (H(2)O(2)). Depending on its local concentration and environment, this oxidant can function as a redox signaling molecule or cause stochastic oxidative damage. Currently, it is well-accepted that dysfunctional peroxiso...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8717923/ https://www.ncbi.nlm.nih.gov/pubmed/34977048 http://dx.doi.org/10.3389/fcell.2021.814047 |
_version_ | 1784624613769084928 |
---|---|
author | Li, Hongli Lismont, Celien Revenco, Iulia Hussein, Mohamed A. F. Costa, Cláudio F. Fransen, Marc |
author_facet | Li, Hongli Lismont, Celien Revenco, Iulia Hussein, Mohamed A. F. Costa, Cláudio F. Fransen, Marc |
author_sort | Li, Hongli |
collection | PubMed |
description | Peroxisomes harbor numerous enzymes that can produce or degrade hydrogen peroxide (H(2)O(2)). Depending on its local concentration and environment, this oxidant can function as a redox signaling molecule or cause stochastic oxidative damage. Currently, it is well-accepted that dysfunctional peroxisomes are selectively removed by the autophagy-lysosome pathway. This process, known as “pexophagy,” may serve a protective role in curbing peroxisome-derived oxidative stress. Peroxisomes also have the intrinsic ability to mediate and modulate H(2)O(2)-driven processes, including (selective) autophagy. However, the molecular mechanisms underlying these phenomena are multifaceted and have only recently begun to receive the attention they deserve. This review provides a comprehensive overview of what is known about the bidirectional relationship between peroxisomal H(2)O(2) metabolism and (selective) autophagy. After introducing the general concepts of (selective) autophagy, we critically examine the emerging roles of H(2)O(2) as one of the key modulators of the lysosome-dependent catabolic program. In addition, we explore possible relationships among peroxisome functioning, cellular H(2)O(2) levels, and autophagic signaling in health and disease. Finally, we highlight the most important challenges that need to be tackled to understand how alterations in peroxisomal H(2)O(2) metabolism contribute to autophagy-related disorders. |
format | Online Article Text |
id | pubmed-8717923 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-87179232021-12-31 The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword? Li, Hongli Lismont, Celien Revenco, Iulia Hussein, Mohamed A. F. Costa, Cláudio F. Fransen, Marc Front Cell Dev Biol Cell and Developmental Biology Peroxisomes harbor numerous enzymes that can produce or degrade hydrogen peroxide (H(2)O(2)). Depending on its local concentration and environment, this oxidant can function as a redox signaling molecule or cause stochastic oxidative damage. Currently, it is well-accepted that dysfunctional peroxisomes are selectively removed by the autophagy-lysosome pathway. This process, known as “pexophagy,” may serve a protective role in curbing peroxisome-derived oxidative stress. Peroxisomes also have the intrinsic ability to mediate and modulate H(2)O(2)-driven processes, including (selective) autophagy. However, the molecular mechanisms underlying these phenomena are multifaceted and have only recently begun to receive the attention they deserve. This review provides a comprehensive overview of what is known about the bidirectional relationship between peroxisomal H(2)O(2) metabolism and (selective) autophagy. After introducing the general concepts of (selective) autophagy, we critically examine the emerging roles of H(2)O(2) as one of the key modulators of the lysosome-dependent catabolic program. In addition, we explore possible relationships among peroxisome functioning, cellular H(2)O(2) levels, and autophagic signaling in health and disease. Finally, we highlight the most important challenges that need to be tackled to understand how alterations in peroxisomal H(2)O(2) metabolism contribute to autophagy-related disorders. Frontiers Media S.A. 2021-12-16 /pmc/articles/PMC8717923/ /pubmed/34977048 http://dx.doi.org/10.3389/fcell.2021.814047 Text en Copyright © 2021 Li, Lismont, Revenco, Hussein, Costa and Fransen. 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 Li, Hongli Lismont, Celien Revenco, Iulia Hussein, Mohamed A. F. Costa, Cláudio F. Fransen, Marc The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword? |
title | The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword? |
title_full | The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword? |
title_fullStr | The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword? |
title_full_unstemmed | The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword? |
title_short | The Peroxisome-Autophagy Redox Connection: A Double-Edged Sword? |
title_sort | peroxisome-autophagy redox connection: a double-edged sword? |
topic | Cell and Developmental Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8717923/ https://www.ncbi.nlm.nih.gov/pubmed/34977048 http://dx.doi.org/10.3389/fcell.2021.814047 |
work_keys_str_mv | AT lihongli theperoxisomeautophagyredoxconnectionadoubleedgedsword AT lismontcelien theperoxisomeautophagyredoxconnectionadoubleedgedsword AT revencoiulia theperoxisomeautophagyredoxconnectionadoubleedgedsword AT husseinmohamedaf theperoxisomeautophagyredoxconnectionadoubleedgedsword AT costaclaudiof theperoxisomeautophagyredoxconnectionadoubleedgedsword AT fransenmarc theperoxisomeautophagyredoxconnectionadoubleedgedsword AT lihongli peroxisomeautophagyredoxconnectionadoubleedgedsword AT lismontcelien peroxisomeautophagyredoxconnectionadoubleedgedsword AT revencoiulia peroxisomeautophagyredoxconnectionadoubleedgedsword AT husseinmohamedaf peroxisomeautophagyredoxconnectionadoubleedgedsword AT costaclaudiof peroxisomeautophagyredoxconnectionadoubleedgedsword AT fransenmarc peroxisomeautophagyredoxconnectionadoubleedgedsword |