Ryosuke Sato, PhD
Phone: (504) 988-4364
Room #: M763
PhD: Gifu University, 2005
Hypertension is one of the most prevalent conditions. The renin-angiotensin system (RAS) is known to play important roles in blood pressure control. Since intrarenal RAS is activated in many forms of hypertension, the renal RAS is acknowledged as a key target for clinical and biochemical studies. Recent studies have revealed that RAS and cytokines contribute to the development of hypertension. Therefore, my research interest is elucidation of molecular mechanisms underlying regulation of intrarenal RAS by the cytokine-activated JAK-STAT pathway. In particular, current focus of my research is the effect of SOCSs on intrarenal RAS regulation and its molecular mechanisms.
- Michael Cypress, B.S. – Graduate Student
- Satou R, Miyata K, Katsurada A, Navar LG, Kobori H. Tumor necrosis factor-α suppresses angiotensinogen expression through formation of a p50/p50 homodimer in human renal proximal tubular cells. Am J Physiol Cell Physiol. 2010;299(4):C750-9.
- Kobori H, Ozawa Y, Acres OW, Miyata K, Satou R. Rho-Kinase/Nuclear Factor Kappa Beta/Angiotensinogen Axis in Angiotensin II-Induced Renal Injury. Hypertens Res. 2011; 34(8):976-9.
- Satou R, Miyata K, Gonzalez-Villalobos R, Ingelfinger JR, Navar LG, and Kobori H. Interferon γ biphasically regulates angiotensinogen expression via a JAK-STAT pathway and suppressor of cytokine signaling 1 (SOCS1) in renal proximal tubular cells. FASEB J. 2012; In Press
Recent Publications: A PubMed listing of research publications for Ryosuke Sato, Ph.D.