Ninjurin-1 drives atherosclerosis progression via <i>NF-κB/CXCL-8</i> activation in endothelial cells.

ABSTRACT:

Introduction

Atherosclerosis represents the leading cause of cardiovascular mortality, with persistent inflammation driving residual risk despite lipid-lowering therapies. While Ninjurin-1 (Ninj1) has been implicated in inflammatory diseases, its endothelial-specific role in atherosclerosis remains unclear.

Methods

We conducted integrated molecular, functional, and histological analyses to characterize Ninj1 expression and function in atherosclerosis. Endothelial Ninj1 silencing was performed to assess its effects on NF-κB signaling, CXCL-8 expression, and ox-LDL-induced endothelial dysfunction. In vivo, ApoE-/- mice were treated with the Ninj1 inhibitor mPN12 peptide to evaluate its impact on plaque formation and composition.

Results

Ninj1 silencing in endothe

SUBMITTER: Sun Z 

PROVIDER: S-EPMC12634354 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature