PINK1 Is Dispensable for Mitochondrial Recruitment of Parkin and Activation of Mitophagy in Cardiac Myocytes
Open accessAbstract
Myocyte function and survival relies on the maintenance of a healthy population of mitochondria. The PINK1/Parkin pathway plays an important role in clearing defective mitochondria via autophagy in cells. However, how the PINK1/Parkin pathway regulates mitochondrial quality control and whether it coordinates with other mitophagy pathways are still unclear. Therefore, the objective of this study was to investigate the effect of PINK1-deficiency on mitochondrial quality control in myocytes. Using PINK1-deficient (PINK1-/-) mice, we found that Parkin is recruited to damaged cardiac mitochondria in hearts after treatment with the mitochondrial uncoupler FCCP or after a myocardial infarction even in the absence of PINK1. Parkin recruitment to depolarized mitochondria correlates with increased ubiquitination of mitochondrial proteins and activation of mitophagy in PINK1-/- myocytes. In addition, induction of mitophagy by the atypical BH3-only protein BNIP3 is unaffected by lack of PINK1. Overall, these data suggest that Parkin recruitment to depolarized cardiac mitochondria and subsequent activation of mitophagy is independent of PINK1. Moreover, alternative mechanisms of Parkin activation and pathways of mitophagy remain functional in PINK1-/- myocytes and could compensate for the PINK1 deficiency.
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PINK1 is dispensable for mitochondrial recruitment of Parkin and activation of mitophagy in cardiomyocytes.
“Importantly, PINK1 was recently shown to be dispensable for mitochondrial recruitment of Parkin and activation of mitophagy in cardiomyocytes [135].”
From Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging (2021) · cites this paper as [135]
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References 43 · Cited by 102
- Authors
- Kubli, D. A., Cortez, M. Q., Moyzis, A. G., Najor, R. H., Lee, Y., & Gustafsson, Å. B.
- Affiliations
- University of California San Diego (US)
- Corresponding author
- Gustafsson, Åsa B.
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-06-25
- Volume
- 10
- Issue
- 6
- Pages
- e0130707
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4482400
- OpenAlex
- W1146046970
- Cited by
- 102
- References
- 43
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 6 · 2023: 8 · 2022: 7 · 2021: 12 · 2020: 10 · 2019: 15 · 2018: 8 · 2017: 10 · 2016: 8 · 2015: 3
- FWCI
- 7.58
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- American Heart Association (14EIA18970095)
- U.S. Public Health Service (HL087023, HL085577)
- National Heart, Lung, and Blood Institute (P01HL085577, R01HL101217, HL-101217, HL087023, HL-085577, R01HL087023, T32HL007444)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- PINK1, Parkin, mitophagy, cardiomyocytes, mitochondrial quality control, mitochondrial depolarization, ubiquitination, BNIP3, myocardial infarction, FCCP
- MeSH terms
- PTEN-Induced Putative Kinase, Animals, Membrane Proteins, Mitochondria, Protein Kinases, Mice, Knockout, Mitochondrial Proteins, Myocytes, Cardiac, Ubiquitin-Protein Ligases, Mice, Mitophagy
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