Angiotensin Ii On Vascular Endothelial Cell Integrin ¦Â3 Expression And Transcriptional Regulation

Atherosclerosis (As) is a principal cause of many lethal diseases. However, its mechanism has not been fully elucidated. It has increasingly been regarded that As is a chronic inflammatory process, in which the central event is the dysfunction of arterial wall endothelial cells (EC)and the later proliferation of smooth muscle cells. Numerous studies suggest that normal functioning of the endothelium is critical inlimiting the development of As. A varity of related pathogenic factors somehow lead to endothelial dysfunction, which can elicit a series of cellular interaction that culminate in the lesion of As. Furthermore, endothelial cells injury and dysfunction are the key event at the early stage of atherosclerosis. A valid schema is nevertheless critically important to discovery of molecular strategies for effective and safe intervention in the early stage of As in order to "limit" the early development of the disease.Angiotensin II(AII), the main effector peptide of the renin-angiotensin system, has been known to play an important role in the regulation of blood pressure and body fluid homeostasis. Increasing evidence suggests that AII can lead to vascular wall hypertrophy in part by directly increasing growth factor and cellular matrix synthesis in vascular smooth muscle cells. Furthermore, AII has been implicated as a factor in atherosclerotic vascular wall changes after vascular injury not only via its role in hypertension but also...