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Mammalian mitophagy – from in vitro molecules to in vivo models
The autophagic turnover of mitochondria, termed mitophagy, is thought to play an essential role in not only maintaining the health of the mitochondrial network but also that of the cell and organism as a whole. We have come a long way in identifying the molecular components required for mitophagy th...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5947125/ https://www.ncbi.nlm.nih.gov/pubmed/29151277 http://dx.doi.org/10.1111/febs.14336 |
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author | Rodger, Catherine E. McWilliams, Thomas G. Ganley, Ian G. |
author_facet | Rodger, Catherine E. McWilliams, Thomas G. Ganley, Ian G. |
author_sort | Rodger, Catherine E. |
collection | PubMed |
description | The autophagic turnover of mitochondria, termed mitophagy, is thought to play an essential role in not only maintaining the health of the mitochondrial network but also that of the cell and organism as a whole. We have come a long way in identifying the molecular components required for mitophagy through extensive in vitro work and cell line characterisation, yet the physiological significance and context of these pathways remain largely unexplored. This is highlighted by the recent development of new mouse models that have revealed a striking level of variation in mitophagy, even under normal conditions. Here, we focus on programmed mitophagy and summarise our current understanding of why, how and where this takes place in mammals. |
format | Online Article Text |
id | pubmed-5947125 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-59471252018-05-17 Mammalian mitophagy – from in vitro molecules to in vivo models Rodger, Catherine E. McWilliams, Thomas G. Ganley, Ian G. FEBS J State‐of‐the‐Art Review The autophagic turnover of mitochondria, termed mitophagy, is thought to play an essential role in not only maintaining the health of the mitochondrial network but also that of the cell and organism as a whole. We have come a long way in identifying the molecular components required for mitophagy through extensive in vitro work and cell line characterisation, yet the physiological significance and context of these pathways remain largely unexplored. This is highlighted by the recent development of new mouse models that have revealed a striking level of variation in mitophagy, even under normal conditions. Here, we focus on programmed mitophagy and summarise our current understanding of why, how and where this takes place in mammals. John Wiley and Sons Inc. 2017-12-01 2018-04 /pmc/articles/PMC5947125/ /pubmed/29151277 http://dx.doi.org/10.1111/febs.14336 Text en © 2017 The Authors. The FEBS Journal published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | State‐of‐the‐Art Review Rodger, Catherine E. McWilliams, Thomas G. Ganley, Ian G. Mammalian mitophagy – from in vitro molecules to in vivo models |
title | Mammalian mitophagy – from in vitro molecules to in vivo models |
title_full | Mammalian mitophagy – from in vitro molecules to in vivo models |
title_fullStr | Mammalian mitophagy – from in vitro molecules to in vivo models |
title_full_unstemmed | Mammalian mitophagy – from in vitro molecules to in vivo models |
title_short | Mammalian mitophagy – from in vitro molecules to in vivo models |
title_sort | mammalian mitophagy – from in vitro molecules to in vivo models |
topic | State‐of‐the‐Art Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5947125/ https://www.ncbi.nlm.nih.gov/pubmed/29151277 http://dx.doi.org/10.1111/febs.14336 |
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