Vascular smooth muscle cells (VSMCs) play a complex role in atherosclerosis. Previously, it was believed that VSMC proliferation promoted plaque formation, while VSMCs in advanced plaques were protective. However, recent studies show that VSMCs can undergo phenotypic switching, transforming into macrophage-like cells that promote atherosclerosis. VSMC behavior is influenced by embryological origin, with different populations having distinct responses to disease-related factors. VSMC phenotypic switching, proliferation, migration, apoptosis, and senescence all contribute to plaque development and instability. VSMCs can originate from various cell types, including bone marrow-derived cells, and their fate is influenced by interactions with other cells and the extracellular matrix. Studies using lineage tracing have shown that VSMCs can contribute to atherosclerotic plaques, but their exact role is complex and varies depending on the lesion stage and environment. VSMC apoptosis and senescence promote inflammation and plaque instability, while VSMC proliferation and migration may have reparative roles. Understanding the molecular mechanisms underlying VSMC behavior is critical for developing new therapeutic strategies to prevent and treat atherosclerosis. The role of VSMCs in atherosclerosis is now recognized as multifaceted, with their behavior influenced by multiple factors, including embryological origin, phenotypic switching, and interactions with other cells. This complex interplay highlights the need for further research to fully understand the role of VSMCs in atherosclerosis and to develop targeted therapies.Vascular smooth muscle cells (VSMCs) play a complex role in atherosclerosis. Previously, it was believed that VSMC proliferation promoted plaque formation, while VSMCs in advanced plaques were protective. However, recent studies show that VSMCs can undergo phenotypic switching, transforming into macrophage-like cells that promote atherosclerosis. VSMC behavior is influenced by embryological origin, with different populations having distinct responses to disease-related factors. VSMC phenotypic switching, proliferation, migration, apoptosis, and senescence all contribute to plaque development and instability. VSMCs can originate from various cell types, including bone marrow-derived cells, and their fate is influenced by interactions with other cells and the extracellular matrix. Studies using lineage tracing have shown that VSMCs can contribute to atherosclerotic plaques, but their exact role is complex and varies depending on the lesion stage and environment. VSMC apoptosis and senescence promote inflammation and plaque instability, while VSMC proliferation and migration may have reparative roles. Understanding the molecular mechanisms underlying VSMC behavior is critical for developing new therapeutic strategies to prevent and treat atherosclerosis. The role of VSMCs in atherosclerosis is now recognized as multifaceted, with their behavior influenced by multiple factors, including embryological origin, phenotypic switching, and interactions with other cells. This complex interplay highlights the need for further research to fully understand the role of VSMCs in atherosclerosis and to develop targeted therapies.