Selective degradation of mitochondria by mitophagy
Open accessAbstract
Mitochondria are the essential site of aerobic energy production in eukaryotic cells. Reactive oxygen species (ROS) are an inevitable by-product of mitochondrial metabolism and can cause mitochondrial DNA mutations and dysfunction. Mitochondrial damage can also be the consequence of disease processes. Therefore, maintaining a healthy population of mitochondria is essential to the well-being of cells. Autophagic delivery to lysosomes is the major degradative pathway in mitochondrial turnover, and we use the term mitophagy to refer to mitochondrial degradation by autophagy. Although long assumed to be a random process, increasing evidence indicates that mitophagy is a selective process. This review provides an overview of the process of mitophagy, the possible role of the mitochondrial permeability transition in mitophagy and the importance of mitophagy in turnover of dysfunctional mitochondria.
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Selective removal of damaged mitochondria following oxidative stress has been reported.
“the selective removal of damaged mitochondria, a major source and target of ROS, following oxidative stress has been reported.(Kim, Rodriguez-Enriquez, and Lemasters 2007)”
From Successful aging: Advancing the science of physical independence in older adults (2015) · cites this paper as Kim et al. 2007
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References 77 · Cited by 1,558
- Authors
- Kim, I., Rodriguez-Enriquez, S., & Lemasters, J. J.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Medical University of South Carolina (US)
- Corresponding author
- Lemasters, John J.
- ORCID
- Lemasters, John J.
- Venue
- Archives of Biochemistry and Biophysics
- Publisher
- Elsevier BV
- Published
- 2007-06
- Volume
- 462
- Issue
- 2
- Pages
- 245-253
- ISSN
- 0003-9861 (ISSN-L)
- PMC
- PMC2756107
- OpenAlex
- W2131007152
- Cited by
- 1,558
- References
- 77
- Citations by year
- 2026: 31 · 2025: 35 · 2024: 65 · 2023: 57 · 2022: 67 · 2021: 91 · 2020: 87 · 2019: 101 · 2018: 91 · 2017: 87 · 2016: 100 · 2015: 88 · 2014: 93 · 2013: 99 · 2012: 106
- FWCI
- 10.59
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Archives of Biochemistry and Biophysics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- National Institutes of Health (1c06rr015455-01a1, DK37034)
- National Institute on Alcohol Abuse and Alcoholism (P50AA011605)
- National Institute of Diabetes and Digestive and Kidney Diseases (2-R01 DK37034, R01DK073336, 1 P01 DK59340, P01DK059340, R37DK037034, R01DK037034, P30DK034987)
- National Center for Research Resources (C06 RR-015455, S10RR013689)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- mitophagy, selective autophagy, mitochondrial turnover, mitochondrial dysfunction, reactive oxygen species, mitochondrial permeability transition, lysosomal degradation, mitochondrial DNA mutations, mitochondrial quality control
- MeSH terms
- Animals, Autophagy, Humans, Mitochondria, Models, Biological, Signal Transduction, Reactive Oxygen Species, Mitochondrial Proteins, Apoptosis Regulatory Proteins
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