Myricetin stabilizes PINK1 to activate mitophagy and ameliorate metabolic dysfunction-associated steatotic liver disease - PubMed
5 hours ago
- #PINK1
- #Myricetin
- #Mitophagy
- Myricetin is a bioactive flavonoid from Abelmoschus manihot that shows therapeutic potential for metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, MASH.
- Myricetin treatment ameliorated hepatic steatosis, inflammation, fibrosis, and insulin resistance in mouse models of MASLD/MASH induced by high-fat or GAN diets.
- Transcriptomic analysis revealed enhanced fatty acid β-oxidation and mitochondrial function after myricetin administration.
- Myricetin directly binds to PINK1, stabilizing it on the outer mitochondrial membrane by inhibiting import through TOM40 and cleavage by PARL protease.
- Stabilized PINK1 activates PINK1/Parkin-dependent mitophagy, restoring mitochondrial integrity and quality.
- Silencing PINK1 abolished myricetin's benefits, confirming the mechanism involving PINK1 stabilization and mitophagy activation.