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Mitophagy and Innate Immunity in Infection

Mitochondria have several quality control mechanisms by which they maintain cellular homeostasis and ensure that the molecular machinery is protected from stress. Mitophagy, selective autophagy of mitochondria, promotes mitochondrial quality control by inducing clearance of damaged mitochondria via...

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Detalles Bibliográficos
Autores principales: Cho, Dong-Hyung, Kim, Jin Kyung, Jo, Eun-Kyeong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Korean Society for Molecular and Cellular Biology 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6999710/
https://www.ncbi.nlm.nih.gov/pubmed/31999918
http://dx.doi.org/10.14348/molcells.2020.2329
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author Cho, Dong-Hyung
Kim, Jin Kyung
Jo, Eun-Kyeong
author_facet Cho, Dong-Hyung
Kim, Jin Kyung
Jo, Eun-Kyeong
author_sort Cho, Dong-Hyung
collection PubMed
description Mitochondria have several quality control mechanisms by which they maintain cellular homeostasis and ensure that the molecular machinery is protected from stress. Mitophagy, selective autophagy of mitochondria, promotes mitochondrial quality control by inducing clearance of damaged mitochondria via the autophagic machinery. Accumulating evidence suggests that mitophagy is modulated by various microbial components in an attempt to affect the innate immune response to infection. In addition, mitophagy plays a key role in the regulation of inflammatory signaling, and mitochondrial danger signals such as mitochondrial DNA translocated into the cytosol can lead to exaggerated inflammatory responses. In this review, we present current knowledge on the functional aspects of mitophagy and its crosstalk with innate immune signaling during infection. A deeper understanding of the role of mitophagy could facilitate the development of more effective therapeutic strategies against various infections.
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spelling pubmed-69997102020-02-12 Mitophagy and Innate Immunity in Infection Cho, Dong-Hyung Kim, Jin Kyung Jo, Eun-Kyeong Mol Cells Minireview Mitochondria have several quality control mechanisms by which they maintain cellular homeostasis and ensure that the molecular machinery is protected from stress. Mitophagy, selective autophagy of mitochondria, promotes mitochondrial quality control by inducing clearance of damaged mitochondria via the autophagic machinery. Accumulating evidence suggests that mitophagy is modulated by various microbial components in an attempt to affect the innate immune response to infection. In addition, mitophagy plays a key role in the regulation of inflammatory signaling, and mitochondrial danger signals such as mitochondrial DNA translocated into the cytosol can lead to exaggerated inflammatory responses. In this review, we present current knowledge on the functional aspects of mitophagy and its crosstalk with innate immune signaling during infection. A deeper understanding of the role of mitophagy could facilitate the development of more effective therapeutic strategies against various infections. Korean Society for Molecular and Cellular Biology 2020-01 2020-01-29 /pmc/articles/PMC6999710/ /pubmed/31999918 http://dx.doi.org/10.14348/molcells.2020.2329 Text en © The Korean Society for Molecular and Cellular Biology. All rights reserved. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-sa/3.0/.
spellingShingle Minireview
Cho, Dong-Hyung
Kim, Jin Kyung
Jo, Eun-Kyeong
Mitophagy and Innate Immunity in Infection
title Mitophagy and Innate Immunity in Infection
title_full Mitophagy and Innate Immunity in Infection
title_fullStr Mitophagy and Innate Immunity in Infection
title_full_unstemmed Mitophagy and Innate Immunity in Infection
title_short Mitophagy and Innate Immunity in Infection
title_sort mitophagy and innate immunity in infection
topic Minireview
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6999710/
https://www.ncbi.nlm.nih.gov/pubmed/31999918
http://dx.doi.org/10.14348/molcells.2020.2329
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