REDD1-dependent GSK3β signaling in podocytes promotes canonical NF-κB activation in diabetic nephropathy.

ABSTRACT: Increasing evidence supports the role of an augmented immune response in the early development and progression of renal complications caused by diabetes. We recently demonstrated that podocyte-specific expression of stress response protein regulated in development and DNA damage response 1 (REDD1) contributes to activation of the pro-inflammatory transcription factor NF-κB in the kidney of diabetic mice. The studies here were designed to define the specific signaling events whereby REDD1 promotes NF-κB activation in the context of diabetic nephropathy. Streptozotocin (STZ)-induced diabetes promoted activation of glycogen synthase kinase 3β (GSK3β) in the kidney, which was prevented by REDD1 ablation. REDD1 was necessary and sufficient to enhance GSK3β activity in human podocyte cultures ex

SUBMITTER: Sunilkumar S 

PROVIDER: S-EPMC11904504 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature