Retinol saturase in the mitochondria antagonizes IDH2 and GLUD1 acetylation to mediate heart repair - PubMed
4 hours ago
- #Cardiac Regeneration
- #Protein Acetylation
- #Mitochondrial Function
- Retsat upregulation in cardiomyocytes occurs during cardiac regeneration in mice.
- Cardiomyocyte-specific Retsat knockin promotes regeneration and improves function after injury; knockout inhibits regeneration.
- Retsat drives cardiomyocyte proliferation independently of its classical retinol saturase activity in the ER.
- Retsat also localizes in mitochondria, and mitochondrial-specific overexpression stimulates proliferation and heart repair.
- Retsat in mitochondria antagonizes IDH2 and GLUD1 acetylation, reducing acetylation levels and enhancing their activities.
- Retsat enters mitochondria by interacting with Tom70 and Tim23 proteins.
- Targeting Retsat is a promising strategy for promoting cardiac regeneration after heart injury.