REDD1 deficiency alleviates podocyte PANoptosis and restores autophagy in diabetic kidney disease - PubMed
3 hours ago
- #autophagy restoration
- #diabetic kidney disease
- #podocyte PANoptosis
- REDD1 deficiency in diabetic mice improved kidney function and reduced podocyte loss and PANoptosis markers.
- Knocking down REDD1 in podocytes suppressed high glucose-induced PANoptosis, mitochondrial damage, and cytoskeletal disorganization.
- REDD1 deletion restored autophagy and TFEB expression in diabetic kidneys and promoted TFEB nuclear translocation in podocytes.
- REDD1 knockout inhibited stratifin (SFN) expression, and SFN knockdown or RIPK3 inhibitor GSK-872 alleviated PANoptosis and autophagy dysfunction.
- SFN overexpression reversed the protective effects of REDD1 knockdown on PANoptosis and autophagy in high glucose conditions.
- The study suggests REDD1 as a potential therapeutic target to slow diabetic kidney disease progression by inhibiting podocyte PANoptosis and restoring autophagy.