Aortic aneurysm and aortic dissection (AA/AD) are critical aortic diseases with a hidden onset and sudden rupture, usually resulting in an inevitable death. Several pro- and anti-angiogenic factors that induce new capillary formation in the existing blood vessels regulate angiogenesis. In addition, aortic disease mainly manifests as the proliferation and migration of endothelial cells of the adventitia vasa vasorum. An increasing number of studies have shown that angiogenesis is a characteristic change that may promote AA/AD occurrence, progression, and rupture. Furthermore, neocapillaries are leaky and highly susceptible to injury by cytotoxic agents, which promote extracellular matrix remodeling, facilitate inflammatory cell infiltration, and release coagulation factors and proteases within the wall. Mechanistically, inflammation, hypoxia, and angiogenic factor signaling play important roles in angiogenesis in AA/AD under the complex interaction of multiple cell types, such as smooth muscle cells, fibroblasts, macrophages, mast cells, and neutrophils. Therefore, based on current evidence, this review aims to discuss the manifestation, pathological role, and underlying mechanisms of angiogenesis involved in AA/AD, providing insights into the prevention and treatment of AA/AD.