Molecular mechanisms of HCMV-driven vascular remodeling and its significance in cardiovascular diseases.

Vascular remodeling, characterazied by dynamic structural and functional adaptations of blood vessels, is pivotal in the pathogenesis of various cardiovascular diseases. Its key processes include endothelial dysfunction, smooth muscle cell proliferation and migration, extracellular matrix metabolism dysregulation and abnormal angiogenesis. Human cytomegalovirus (HCMV), a prevalent herpesvirus, establishes latent infections in immunocompetent individuals and reactives in immunocompromised states. Accumulating evidence indicates that HCMV infection is closely linked to vascular remodeling: it disrupts the balance between vascular cell proliferation and apoptosis by regulating host cell cycle-related genes. Moreover, HCMV modulates G protein-coupled signaling through viral GPCR homologs or early proteins regulating host GPCR expression and downstream molecules, thereby affecting cytokine expression and signaling pathways. This review summarizes the elucidated mechanisms by which HCMV promotes vascular remodeling, aiming to provide directions for future studies on how this virus affects cell functions and vascular dynamics, and offer references for the treatment of related diseases.