The 103rd Annual Meeting of The Physiological Society of Japan

Chairperson:Kazutaka Ueda (International University of Health and Welfare)

Co-sponsored:Nippi, Incorporated

The aorta maintains vascular wall homeostasis by conferring elasticity and tensile strength through elastic fibers and collagen fibers, respectively. Congenital or acquired fragility of the aortic wall disrupts the mechanical stress responses of smooth muscle cells, leading to the development of aortic aneurysms. We have reported that the matricellular protein thrombospondin-1 functions as a mechanical stress–responsive factor and contributes to the maintenance of the aortic wall via the integrin–YAP signaling pathway. Aortic dissection, on the other hand, is a disease characterized by aortic rupture and organ malperfusion, and is a major cause of sudden death at a young age in conditions such as Marfan syndrome. However, the mechanisms underlying the initiation and progression of aortic dissection remain largely unknown. In this seminar, we will introduce mouse models of aortic aneurysm and aortic dissection that we have established, discuss their molecular pathological basis, and explore how these findings may be translated into future therapeutic strategies.