Acarbose ameliorates podocyte injury and glomerular lesions in diabetic nephropathy through USP46 activation - PubMed
14 hours ago
- #Diabetic Nephropathy
- #USP46
- #Acarbose
- Acarbose improves podocyte injury and glomerular lesions in diabetic nephropathy by activating USP46.
- Patients with diabetic nephropathy show lower USP46 expression in podocytes, associated with higher proteinuria.
- Usp46 gene deletion in mice (Usp46PKO) leads to spontaneous albuminuria and worsens podocyte injury under diabetic conditions.
- Loss of USP46 causes TDP-43 aggregation and cytosolic translocation in podocytes.
- Acarbose acts as a USP46 agonist, reducing TDP-43 aggregation, preventing podocyte loss, and mitigating albuminuria in diabetic mice.
- The therapeutic effects of acarbose are nullified in Usp46PKO mice, highlighting USP46's role.
- This study suggests acarbose's potential therapeutic benefits in diabetic nephropathy beyond glucose regulation.