CAP1 deficiency protects podocytes in diabetic kidney disease by reducing mitochondria-associated endoplasmic reticulum membrane formation and mitochondrial fission - PubMed
4 hours ago
- #podocyte injury
- #mitochondrial fission
- #diabetic kidney disease
- CAP1 deficiency protects podocytes in diabetic kidney disease (DKD) by reducing mitochondria-associated endoplasmic reticulum membrane (MAM) formation and mitochondrial fission.
- Excessive mitochondrial fission is an early pathological event in podocyte injury in DKD.
- Podocyte-specific CAP1 knockdown ameliorates podocyte injury and albuminuria in diabetic mice by inhibiting MAM formation and mitochondrial fission.
- High glucose triggers CAP1-induced actin depolymerization, promoting INF2 enrichment from the ER to the MAM.
- Enhanced interaction between CAP1 and INF2 at the MAM interface exacerbates mitochondrial fission and dysfunction, leading to podocyte injury.
- First evidence of CAP1's pathogenic role in podocytes during DKD progression and its mechanism via MAM.