Vascular fibrosis is the core pathological process of cardiovascular disease progression, which is characterized by abnormal deposition and remodeling of extracellular matrix (ECM) in the vascular wall. This results in the loss of vascular elasticity, hemodynamic derangement, and end-organ damage. This process involves the phenotypic transformation of vascular smooth muscle cell (VSMC), endothelial-mesenchymal transition (EndMT), and activation of inflammatory-fibrotic networks. The mechanisms include multicellular interactions, signaling pathway crosstalk, and epigenetic regulation. This article systematically reviews the pathophysiological basis, key molecules and signaling networks of vascular fibrosis, discusses potential therapeutic targets and clinical translation challenges based on current research status, and provides an outlook on future development directions.