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Mitophagy and Neuroinflammation: A Compelling Interplay
Mitochondria are the main sites of energy production and a major source of metabolic stress. Not surprisingly, impairment of mitochondrial homeostasis is strongly associated with the development and progression of a broad spectrum of human pathologies, including neurodegenerative disorders. Mitophag...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Bentham Science Publishers
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10472808/ https://www.ncbi.nlm.nih.gov/pubmed/35762540 http://dx.doi.org/10.2174/1570159X20666220628153632 |
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author | Charmpilas, Nikolaos Fang, Evandro Fei Palikaras, Konstantinos |
author_facet | Charmpilas, Nikolaos Fang, Evandro Fei Palikaras, Konstantinos |
author_sort | Charmpilas, Nikolaos |
collection | PubMed |
description | Mitochondria are the main sites of energy production and a major source of metabolic stress. Not surprisingly, impairment of mitochondrial homeostasis is strongly associated with the development and progression of a broad spectrum of human pathologies, including neurodegenerative disorders. Mitophagy mediates the selective degradation of damaged organelles, thus promoting cellular viability and tissue integrity. Defective mitophagy triggers cellular senescence and prolonged neuroinflammation, leading eventually to cell death and brain homeostasis collapse. Here, we survey the intricate interplay between mitophagy and neuroinflammation, highlighting that mitophagy can be a focal point for therapeutic interventions to tackle neurodegeneration. |
format | Online Article Text |
id | pubmed-10472808 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Bentham Science Publishers |
record_format | MEDLINE/PubMed |
spelling | pubmed-104728082023-11-18 Mitophagy and Neuroinflammation: A Compelling Interplay Charmpilas, Nikolaos Fang, Evandro Fei Palikaras, Konstantinos Curr Neuropharmacol Medicine, Neurology, Pharmacology, Neuroscience Mitochondria are the main sites of energy production and a major source of metabolic stress. Not surprisingly, impairment of mitochondrial homeostasis is strongly associated with the development and progression of a broad spectrum of human pathologies, including neurodegenerative disorders. Mitophagy mediates the selective degradation of damaged organelles, thus promoting cellular viability and tissue integrity. Defective mitophagy triggers cellular senescence and prolonged neuroinflammation, leading eventually to cell death and brain homeostasis collapse. Here, we survey the intricate interplay between mitophagy and neuroinflammation, highlighting that mitophagy can be a focal point for therapeutic interventions to tackle neurodegeneration. Bentham Science Publishers 2023-05-18 2023-05-18 /pmc/articles/PMC10472808/ /pubmed/35762540 http://dx.doi.org/10.2174/1570159X20666220628153632 Text en © 2023 Bentham Science Publishers https://creativecommons.org/licenses/by/4.0/© 2023 The Author(s). Published by Bentham Science Publisher. This is an open access article published under CC BY 4.0 https://creativecommons.org/licenses/by/4.0/legalcode) |
spellingShingle | Medicine, Neurology, Pharmacology, Neuroscience Charmpilas, Nikolaos Fang, Evandro Fei Palikaras, Konstantinos Mitophagy and Neuroinflammation: A Compelling Interplay |
title | Mitophagy and Neuroinflammation: A Compelling Interplay |
title_full | Mitophagy and Neuroinflammation: A Compelling Interplay |
title_fullStr | Mitophagy and Neuroinflammation: A Compelling Interplay |
title_full_unstemmed | Mitophagy and Neuroinflammation: A Compelling Interplay |
title_short | Mitophagy and Neuroinflammation: A Compelling Interplay |
title_sort | mitophagy and neuroinflammation: a compelling interplay |
topic | Medicine, Neurology, Pharmacology, Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10472808/ https://www.ncbi.nlm.nih.gov/pubmed/35762540 http://dx.doi.org/10.2174/1570159X20666220628153632 |
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