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Abstract
Mutations in PINK1 and PRKN disrupt mitochondrial quality control pathways and are linked to early-onset Parkinson's disease.
- Mitophagy and mitochondrial quality control are essential for cellular health and neuronal function.
- PINK1-dependent recruitment of Parkin to damaged mitochondria has been well-established.
- Recent advances have clarified the mechanisms that activate PINK1 and Parkin and their roles in cellular signaling.
- There is regulatory crosstalk between mitophagy and other cellular stress responses.
- The PINK1/Parkin pathway may serve as a potential therapeutic target for Parkinson's disease.
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