Integrated multi‐omics analysis reveals metabolic reprogramming as a key driver of angiotensin II‐induced vascular remodeling

Abstract Vascular remodeling is a prominent pathological characteristic of cardiovascular diseases (CVDs), with angiotensin II (Ang II) known to induce vascular injury and remodeling by modulating the functions of vascular smooth muscle cells (SMCs). However, the precise mechanisms underlying this process remain incompletely understood. In this study, we established a primary human aortic SMC model and employed a multi‐omics approach—including untargeted proteomics, lipidomics, and metabolomics through mass spectrometry (MS)—to investigate the molecular alterations induced by Ang II. By integrating omics data from Ang II‐treated and control groups, we identified significantly altered molecules and pathways that reflect functional changes and cellular inflammation in SMCs. Subsequent pathway enrichment and interaction network analyses of proteomics and metabolomics datasets revealed critical pathways involved in Ang II‐induced vascular remodeling. Our findings highlight metabolic reprogramming and oxidative stress responses in SMCs following Ang II exposure, emphasizing their role in regulating vascular remodeling. These insights provide a comprehensive understanding of the molecular events driving vascular remodeling and open new avenues for targeted therapeutic interventions in CVDs.