A CPEB2/ANGPTL3 feedback loop promotes the progression of podocyte injury in nephrotic syndrome.

ABSTRACT: Podocyte injury is the primary pathology responsible for 70-90% of nephrotic syndrome (NS) in children, a condition closely associated with the aberrant expression of Angiopoietin-like-3 (ANGPTL3). The regulatory mechanism by which ANGPTL3 is upregulated during NS progression remains elusive. In this study, we found that ANGPTL3 can be regulated by Cytoplasmic polyadenylation element binding protein 2 (CPEB2) through translational control, and conversely, CPEB2 can be transcriptionally regulated in response to ANGPTL3 signaling as a feedback loop. Exposure to puromycin aminonucleoside (PAN) or adriamycin (ADR) dose-dependently increased the expression of both CPEB2 and ANGPTL3 in MPC-5 cells. Ectopic overexpression of CPEB2 in MPC-5 cells significantly promoted cell apoptosis and migration

SUBMITTER: Zheng X 

PROVIDER: S-EPMC12606126 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature