Fibroblast Growth Factor 21 Promotes Vascular Smooth Muscle Cell Contractile Polarization via p38 Mitogen-Activated Protein Kinase-Promoted Serum Response Factor Phosphorylation.

ABSTRACT: Phenotypic abnormalities in vascular smooth muscle cells (VSMCs) are believed to play essential roles in the progression of vascular diseases. Here, we explored the impact of fibroblast growth factor 21 (FGF21) on the phenotypic transition of VSMCs. Our findings revealed that FGF21 expression was substantially down-regulated in both human and mouse neointimal regions. Additionally, plasma FGF21 levels were lower in patients with atherosclerotic coronary artery disease (ASCAD) compared to those without ASCAD. Similarly, patients with restenosis exhibited reduced FGF21 levels compared to those without restenosis. In vivo, FGF21 deficiency accelerated intimal hyperplasia and decreased the number of contractile VSMCs in mouse neointima. However, hepatocyte-specific FGF21 knockout had no effect

SUBMITTER: Zhu M 

PROVIDER: S-EPMC12324144 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature