Aortic aneurysm and dissection (AAD) represent a life-threatening aortic disorder, for which current treatment strategies rely predominantly on surgical interventions, with limited pharmacological options targeting the underlying pathophysiology. Vascular smooth muscle cell (VSMC) dysfunction constitutes a central pathological mechanism in the development and progression of AAD. This review outlines the association between VSMCs and AAD, covering their physiological functions and pathological alterations, including phenotypic switching, cell death, and VSMC-mediated extracellular matrix remodeling. It further discusses the impact of epigenetic modifications on VSMC core functions. Additionally, this review addresses normal energy metabolism pathways of VSMCs and the mechanisms of metabolic reprogramming, as well as abnormalities in amino acid metabolism, lipid metabolism, and other metabolic pathways. Signaling mechanisms related to AMPK activation and mitochondrial function are also highlighted. Currently, AAD management is dominated by surgical interventions, while pharmacological therapy remains limited to symptomatic control. Looking ahead, future research should focus on VSMC metabolism-related mechanisms to develop early prevention strategies and novel targeted therapeutics, thereby improving the current treatment landscape for AAD.

Coronary artery disease (CAD) remains a major cause of morbidity and mortality worldwide, imposing a substantial burden on patients and healthcare systems. Its development and progression are driven not only by lipid accumulation and inflammation but also by extracellular matrix remodeling. Collagen is a core component of the cardiovascular extracellular matrix. Its subtype composition, maturation, cross-linking, synthesis and degradation collectively shape the structural and functional properties of vascular and myocardial tissues. Here, we review collagen biology and use expression profiles from GTEx v11 and Heart Cell Atlas v2 to illustrate tissue- and cell type-specific patterns. These profiles illustrate the expression patterns and major cellular sources of the collagen gene family in the coronary artery and left ventricle. We also evaluate evidence linking collagen-related genetic variation to CAD susceptibility. By connecting genetic variation with protein processing and tissue architecture, this review delineates the potential roles of collagen in plaque stability, coronary thrombosis and post-infarction myocardial remodeling. This framework provides a basis for developing biomarkers of collagen remodeling and mechanism-guided therapeutic strategies.