TMEM106A mediates atherosclerosis progression through macrophage-centered immune responses and chemokine signaling.

ABSTRACT:

Background

Atherosclerosis (AS) remains a leading cause of cardiovascular morbidity and mortality, characterized by intricate interactions between immune dysregulation and lipid metabolism abnormalities-identifying key mediators in its pathogenesis is critical for improving diagnostics and therapies. This study focuses on Transmembrane Protein 106A (TMEM106A) to clarify its role and clinical relevance in AS progression.

Methods

Public transcriptomic datasets (GSE43292, GSE100927, GSE28829) were analyzed to assess TMEM106A expression and diagnostic value; single-cell RNA-seq data (GSE159677) defined its cellular localization. Immune infiltration (ssGSEA, Cibersort, xCell) and CellChat (intercellular communication) analyses explored its immune associations. In vivo vali

SUBMITTER: Gao M 

PROVIDER: S-EPMC12741138 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature