Molecular mechanisms and physiological functions of mitophagy
Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conju...
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| Published in: | The EMBO journal Vol. 40; no. 3; pp. e104705 - n/a |
|---|---|
| Main Authors: | , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
London
Nature Publishing Group UK
01.02.2021
Springer Nature B.V John Wiley and Sons Inc |
| Subjects: | |
| ISSN: | 0261-4189, 1460-2075, 1460-2075 |
| Online Access: | Get full text |
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| Abstract | Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy‐mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy
in vivo
also reveal high rates of steady‐state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations.
Graphical Abstract
This review describes the conserved pathways for mitochondrial degradation via selective autophagy across species, and how multiple mitophagy pathways cooperate to modulate mitochondrial fitness and number in normal or disease physiology. |
|---|---|
| AbstractList | Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy-mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady-state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations.Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy-mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady-state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations. Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy‐mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady‐state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations. Graphical Abstract This review describes the conserved pathways for mitochondrial degradation via selective autophagy across species, and how multiple mitophagy pathways cooperate to modulate mitochondrial fitness and number in normal or disease physiology. Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy‐mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady‐state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations. Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy‐mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady‐state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations. This review describes the conserved pathways for mitochondrial degradation via selective autophagy across species, and how multiple mitophagy pathways cooperate to modulate mitochondrial fitness and number in normal or disease physiology. Degradation of mitochondria via a selective form of autophagy, named mitophagy, is a fundamental mechanism conserved from yeast to humans that regulates mitochondrial quality and quantity control. Mitophagy is promoted via specific mitochondrial outer membrane receptors, or ubiquitin molecules conjugated to proteins on the mitochondrial surface leading to the formation of autophagosomes surrounding mitochondria. Mitophagy‐mediated elimination of mitochondria plays an important role in many processes including early embryonic development, cell differentiation, inflammation, and apoptosis. Recent advances in analyzing mitophagy in vivo also reveal high rates of steady‐state mitochondrial turnover in diverse cell types, highlighting the intracellular housekeeping role of mitophagy. Defects in mitophagy are associated with various pathological conditions such as neurodegeneration, heart failure, cancer, and aging, further underscoring the biological relevance. Here, we review our current molecular understanding of mitophagy, and its physiological implications, and discuss how multiple mitophagy pathways coordinately modulate mitochondrial fitness and populations. This review describes the conserved pathways for mitochondrial degradation via selective autophagy across species, and how multiple mitophagy pathways cooperate to modulate mitochondrial fitness and number in normal or disease physiology. |
| Author | Okamoto, Koji Yamano, Koji Onishi, Mashun Matsuda, Noriyuki Sato, Miyuki |
| AuthorAffiliation | 2 The Ubiquitin Project Tokyo Metropolitan Institute of Medical Science Tokyo Japan 1 Laboratory of Mitochondrial Dynamics Graduate School of Frontier Biosciences Osaka University Suita Japan 3 Laboratory of Molecular Membrane Biology Institute for Molecular and Cellular Regulation Gunma University Maebashi Japan |
| AuthorAffiliation_xml | – name: 1 Laboratory of Mitochondrial Dynamics Graduate School of Frontier Biosciences Osaka University Suita Japan – name: 3 Laboratory of Molecular Membrane Biology Institute for Molecular and Cellular Regulation Gunma University Maebashi Japan – name: 2 The Ubiquitin Project Tokyo Metropolitan Institute of Medical Science Tokyo Japan |
| Author_xml | – sequence: 1 givenname: Mashun orcidid: 0000-0003-1511-4097 surname: Onishi fullname: Onishi, Mashun organization: Laboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University – sequence: 2 givenname: Koji orcidid: 0000-0002-4692-161X surname: Yamano fullname: Yamano, Koji organization: The Ubiquitin Project, Tokyo Metropolitan Institute of Medical Science – sequence: 3 givenname: Miyuki orcidid: 0000-0002-1944-4918 surname: Sato fullname: Sato, Miyuki email: m-sato@gunma-u.ac.jp organization: Laboratory of Molecular Membrane Biology, Institute for Molecular and Cellular Regulation, Gunma University – sequence: 4 givenname: Noriyuki orcidid: 0000-0001-8199-952X surname: Matsuda fullname: Matsuda, Noriyuki email: matsuda-nr@igakuken.or.jp organization: The Ubiquitin Project, Tokyo Metropolitan Institute of Medical Science – sequence: 5 givenname: Koji orcidid: 0000-0003-4730-4522 surname: Okamoto fullname: Okamoto, Koji email: kokamoto@fbs.osaka-u.ac.jp organization: Laboratory of Mitochondrial Dynamics, Graduate School of Frontier Biosciences, Osaka University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33438778$$D View this record in MEDLINE/PubMed |
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| Keywords | autophagy phosphorylation mitochondria quality and quantity control ubiquitin |
| Language | English |
| License | Attribution 2021 The Authors. Published under the terms of the CC BY 4.0 license. 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. |
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