The hemodynamics within the aortic lumen are highly complex, and the mechanical stimuli generated by blood flow play a crucial role in the occurrence and progression of aortic dilation disease. Endothelial cells, as key components of the vascular endothelium, respond precisely to microenvironmental changes caused by blood flow through mechanoreceptors, including ion channels, receptor tyrosine kinases, and membrane structures. These mechanoreceptors convert mechanical stress into biochemical signals, thereby affecting the physiological functions and pathological changes of blood vessels. In recent years, significant advances have been made in understanding the mechanisms by which endothelial mechanoreceptors are involved in aortic dilation disease. This article summarizes the research progress of mechanoreceptor-mediated endothelial cell function in regulating aortic dilation disease and provides a perspective on future research directions, with the aim of offering new insights and potential targets for the development of clinical treatment strategies.