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Mitophagy: mechanisms, pathophysiological roles, and analysis
Open accessAbstract
Mitochondria are essential organelles that regulate cellular energy homeostasis and cell death. The removal of damaged mitochondria through autophagy, a process called mitophagy, is thus critical for maintaining proper cellular functions. Indeed, mitophagy has been recently proposed to play critical roles in terminal differentiation of red blood cells, paternal mitochondrial degradation, neurodegenerative diseases, and ischemia or drug-induced tissue injury. Removal of damaged mitochondria through autophagy requires two steps: induction of general autophagy and priming of damaged mitochondria for selective autophagic recognition. Recent progress in mitophagy studies reveals that mitochondrial priming is mediated either by the Pink1-Parkin signaling pathway or the mitophagic receptors Nix and Bnip3. In this review, we summarize our current knowledge on the mechanisms of mitophagy. We also discuss the pathophysiological roles of mitophagy and current assays used to monitor mitophagy.
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“The PINK1/Parkin) pathway is among the best characterized pathways through which mitophagy is induced in mammalian cells[28]”
From Overexpression of pink1 or parkin in indirect flight muscles promotes mitochondrial proteostasis and extends lifespan in Drosophila melanogaster (2019) · cites this paper as [28]
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Self-citation
Metadata
- Authors
- Ding, W.-X., & Yin, X.-M.
- Affiliations
- University of Kansas Medical Center (US)
- Indiana University School of Medicine (US)
- Venue
- bchm
- Publisher
- Walter de Gruyter GmbH
- Published
- 2012-07-01
- Volume
- 393
- Issue
- 7
- Pages
- 547-564
- ISSN
- 1431-6730 (ISSN-L)
- 1437-4315
- PMC
- PMC3630798
- OpenAlex
- W2076769172
- Cited by
- 1,032
- References
- 166
- Citations by year
- 2026: 47 · 2025: 77 · 2024: 83 · 2023: 99 · 2022: 90 · 2021: 115 · 2020: 111 · 2019: 98 · 2018: 67 · 2017: 64 · 2016: 59 · 2015: 44 · 2014: 50 · 2013: 25 · 2012: 1
- FWCI
- 4.79
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Biological Chemistry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Funders
- National Institutes of Health (AA020518, RR016475)
- National Institute on Alcohol Abuse and Alcoholism (R01AA020518, R21AA017421, R37AA020518)
- National Cancer Institute (R01CA83817, R01CA083817)
- National Institute of General Medical Sciences (P20GM103418)
- National Center for Research Resources (P20RR021940, RR016475, P20RR016475)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- mitophagy, PINK1/Parkin pathway, Nix, BNIP3, mitochondrial priming, selective autophagy, neurodegenerative diseases, ischemia, energy homeostasis, cell death
- MeSH terms
- Aging, Animals, Disease, Humans, Mitochondria, Signal Transduction, Mitochondrial Proteins, Mitophagy
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