The role of EVs in VC development associated with vascular senescence. Under physiological conditions, the vasculature presents a balance between oxidative stress, inflammatory factors, and calcium and phosphate release and highlights the regular release of extracellular vesicles. All these mediators are focused on maintaining vessel homeostasis. The loss of homeostasis could appear with physiological aging and age-related pathologies such as CKD and/or CVD, which implies the imbalance of several processes. Both physiological and premature aging illnesses are characterized by an increase in ROS, calcium, and phosphate release, inflammatory mediators, adhesion molecules, coagulation process, the proliferation of extracellular matrix proliferation in the blood, and especially increased vasculature senescence. In addition, cells from a senescent vessel, especially endothelial cells and vascular smooth muscle cells, release extracellular vesicles that contain calcification factors. Complex signaling pathways in senescent extracellular vesicles cause spontaneous calcium ion precipitation in the arteries and thus contribute to VC development and pathophysiology.