Vascular aging is an independent risk factor for cardio-cerebrovascular diseases. DNA methylation, as an important epigenetic regulatory mechanism, participates in the process of vascular aging through multiple pathways. First, DNA methylation can regulate the oxidative stress response, leading to excessive generation of reactive oxygen species (ROS), which damages vascular endothelial cells. Second, it can also induce inflammatory responses, promote the release of inflammatory factors, and disrupt vascular homeostasis. Furthermore, DNA methylation can affect telomere and mitochondrial function by interfering with telomerase activity and mitochondrial energy metabolism, thereby accelerating the aging process of vascular cells. These pathophysiological mechanisms interact and synergize in vivo, collectively promoting vascular aging and contributing to the development of various cardiovascular events, such as coronary heart disease, hypertension, and ischemic stroke. Therefore, DNA methylation plays an important role in promoting vascular aging and represents a key target for the prevention and treatment of aging-related cardio-cerebrovascular diseases.