Identification of central regulatory hubs in the molecular interaction network underlying cardiac fibroblast-to-myofibroblast transition

Abstract

Cardiac fibrosis is a pathological process characterized by excessive accumulation of extracellular matrix components, leading to structural and functional impairment of the heart. A key event in this process is the transition of cardiac fibroblasts into myofibroblasts, which are responsible for increased extracellular matrix production and tissue remodeling. The aim of this study was to identify molecular mechanisms involved in fibroblast-to-myofibroblast transition using bioinformatic analysis. A protein–protein interaction network was constructed based on genes associated with cardiac fibrosis and functional enrichment analysis was performed. The results identified TGF-β signaling, extracellular matrix remodeling, inflammatory response and mechanotransduction as the major biological processes involved in fibroblast activation and fibrosis progression. These findings highlight the complex molecular network regulating cardiac fibrosis and indicate potential targets for future therapeutic strategies.