TEAD1-Mediated Trans-Differentiation of Vascular Smooth Muscle Cells into Fibroblast-Like Cells Contributes to the Stabilization and Repair of Disrupted Atherosclerotic Plaques.

ABSTRACT: Atherosclerotic plaque rupture mainly contributes to acute coronary syndrome (ACS). Insufficient repair of these plaques leads to thrombosis and subsequent ACS. Central to this process is the modulation of vascular smooth muscle cells (VSMCs) phenotypes, emphasizing their pivotal role in atherosclerotic plaque stability and healing post-disruption. Here, an expansion of FSP1⁺ cells in a tandem stenosis (TS) model of atherosclerotic mice is unveiled, predominantly originating from VSMCs through single-cell RNA sequencing (scRNA-seq) analyses and VSMC lineage tracing studies. Further investigation identified TEA domain transcription factor 1 (TEAD1) as the key transcription factor driving the trans-differentiation of VSMCs into fibroblast-like cells. In vivo experiments using a TS

SUBMITTER: Zhai M 

PROVIDER: S-EPMC11791998 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature