PINK1 Is Dispensable for Mitochondrial Recruitment of Parkin and Activation of Mitophagy in Cardiac Myocytes
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Summary
It is 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, and alternative mechanisms of Parkin activation and pathways of mitophagy remain functional in Pink1-/- myocytes and could compensate for the PINK 1 deficiency.
- Type
- article
- Published
- 2015-06-25
- Cited by
- 98
- References
- 43
- Access
- Open access
- OpenAlex
- https://openalex.org/W1146046970
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:18957793
Keywords
Mitophagy, PINK1, Parkin, Mitochondrion, Cell biology
References
- Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism
- Mitophagy Is Required for Acute Cardioprotection by Simvastatin
- Mitochondria as sensors and regulators of calcium signalling
- PTEN-inducible kinase 1 (PINK1)/Park6 is indispensable for normal heart function
- The PINK1/Parkin pathway regulates mitochondrial morphology
- Mitochondrial Pruning by Nix and BNip3: An Essential Function for Cardiac-Expressed Death Factors
- Nix Is Critical to Two Distinct Phases of Mitophagy, Reactive Oxygen Species-mediated Autophagy Induction and Parkin-Ubiquitin-p62-mediated Mitochondrial Priming*
- Pink1, the first ubiquitin kinase
- Bnip3 Impairs Mitochondrial Bioenergetics and Stimulates Mitochondrial Turnover
- Molecular Mechanisms of Autophagy in the Cardiovascular System
- Cytosolic p53 inhibits Parkin-mediated mitophagy and promotes mitochondrial dysfunction in the mouse heart
- PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
- Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin
- Ubiquitin is phosphorylated by PINK1 to activate parkin
- A vesicular transport pathway shuttles cargo from mitochondria to lysosomes.
- Parkin is a lipid-responsive regulator of fat uptake in mice and mutant human cells.
- Mitochondrial processing peptidase regulates PINK1 processing, import and Parkin recruitment
- Mitochondria and cell death: outer membrane permeabilization and beyond
- Mitochondrial Quality Control in the Myocardium: Cooperation between Protein Degradation and Mitophagy
- Preconditioning Involves Selective Mitophagy Mediated by Parkin and p62/SQSTM1
Cited by
- Mitochondrial autophagy in cardiomyopathy
- Parkin-dependent mitophagy in the heart
- Mitochondrial Quality Control in the Diabetic Heart
- NDPK-D (NM23-H4)-mediated externalization of cardiolipin enables elimination of depolarized mitochondria by mitophagy
- Mitochondrial biogenesis and dynamics in the developing and diseased heart
- Central Parkin: The evolving role of Parkin in the heart
- Mechanisms of mitophagy: putting the powerhouse into the doghouse
- Redox Biology and the Interface Between Bioenergetics, Autophagy and Circadian Control of Metabolism
- PINK1 is required for timely cell-type specific mitochondrial clearance during Drosophila midgut metamorphosis.
- WDR26 promotes mitophagy of cardiomyocytes induced by hypoxia through Parkin translocation.
- Parkin and PINK1 functions in oxidative stress and neurodegeneration
- PINK1 alleviates myocardial hypoxia-reoxygenation injury by ameliorating mitochondrial dysfunction.
- Beyond Mitophagy: The Diversity and Complexity of Parkin Function
- Mitochondrion: A Common Organelle for Distinct Cell Deaths?
- Emerging role of mitophagy in human diseases and physiology
- Potential signaling pathways of acute endurance exercise-induced cardiac autophagy and mitophagy and its possible role in cardioprotection
- Peptidyl‐Prolyl Isomerase 1 Regulates Ca2+ Handling by Modulating Sarco(Endo)Plasmic Reticulum Calcium ATPase and Na2+/Ca2+ Exchanger 1 Protein Levels and Function
- Mitophagy as a Protective Mechanism against Myocardial Stress
- Examining Autophagy and Mitophagy as Inducible Mechanisms of Cellular Remodelling
- PINK1-PRKN/PARK2 pathway of mitophagy is activated to protect against renal ischemia-reperfusion injury
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- Nix restores mitophagy and mitochondrial function to protect against PINK1/Parkin-related Parkinson’s disease
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- KAT8 compound inhibition inhibits the initial steps of PINK1-dependant mitophagy