Shengyu Mu, M.D., Ph.D.
Phone: (501) 603-1081
Fax: (501) 686-8970
M.D. – TianJin Medical University, TianJin, China, 2004
Ph.D. – The University of Tokyo, Tokyo, Japan, 2011
The primary interest of my research has been focusing on the pathogenesis of hypertension in renal salt-reabsorption and the systemic vasculature. The long-term goal of our laboratory is to understand the mechanism of the development of hypertension and to translate our basic scientific discovery to clinics to contribute to a final cure for hypertension. To accomplish this goal, we have conducted multiple screenings to identify potential pathogenic targets in hypertension. Extending from our initial screen, we are performing laboratory experiments using both pharmacological and genetic approaches to determine the role of the identified molecules in the development of hypertension. Our most recent project is investigating the role and molecular mechanisms of immune cells in stimulating sodium retention in kidney, which contributes to the pathogenesis of salt-sensitive hypertension. In addition, we have acquired techniques and research experience involved in most areas of physiology, biology, molecular genetics, epigenetics, histology and vascular biology that are needed to pursue our goal of translational medicine. I am collaborating with Phil Palade, Ph.D. and Yunmeng Liu, Ph.D. on this research.
Recent Research Support
15BGIA25730047 AHA (PI) (07/01/15 – 06/30/17)
“Role of Immune Cells in kidney in the Development of Salt-Sensitive Hypertension”
Sims CR, Singh SP, Mu S, Gokden N, Zakaria D, Nguyen TC and Mayeux PR. Rolipram Improves Outcome in a Rat Model of Infant Sepsis-Induced Cardiorenal Syndrome. Frontiers in Pharmacology. 8: 237; 2017 (PMID: 28515693).
Liu Y, Rafferty T, Rhee S, Webber J, Song L, Ko B, Hoover R, He B, Mu S. CD8+ T cells stimulate Na-Cl co-transporter NCC in distal convoluted tubules leading to salt-sensitive hypertension. Nat. Commun. 8, 10437; 2017 (PMID: 28067240).
Uetake Y, Ikeda H, Irie R, Tejima K, Matsui H, Ogura S, Wang H, Mu S, Hirohama D, Ando K, Sawamura T, Yatomi Y, Fujita T, Shimosawa T. High-salt in addition to high-fat diet may enhance inflammation and fibrosis in liver steatosis induced by oxidative stress and dyslipidemia in mice. Lipids Health Dis. 14:6, 2014 (PMID: 25888871).
Jimbo R, Kawakami-Mori F, Mu S, Hirohama D, Majtan B, Shimizu Y, Yatomi Y, Fukumoto S, Fujita T, Shimosawa T. Fibroblast growth factor 23 accelerates phosphate-induced vascular calcification in the absence of Klotho deficiency. Kidney Int. 85(5): 1103-11, 2013 (PMID: 24088960).
Ogura S, Shimosawa T, Mu S, Sonobe T, Kawakami-Mori F, Wang H, Uetake Y, Yoshida K, Yatomi Y, Shirai M, Fujita T. Oxidative stress augments pulmonary hypertension in chronically hypoxic mice overexpressing the oxidized LDL receptor. Am J Physiol Heart Circ Physiol. 305(2):H155-62, 2013 (PMID: 23686713).
Mori-Kawakami F, Shimosawa T, Wang H, Ogura S, Mu S, Yatomi Y, Fujita T. NADPH oxidase-mediated Rac1 GTP activity is necessary for non-genomic actions of the mineralocorticoid receptor in the CA1 region of the rat hippocampus. Am J Physiol Endoc Metab. 302(4): E425-32, 2012 (PMID: 22114025).
Shimosawa T, Mu S, Shibata S, Fujita T. The Kidney and Hypertension: Pathogenesis of Salt-Sensitive Hypertension. Curr Hypertens Rep. 14(5): 468-472, 2012 (PMID: 22752520).
Shibata S*, Mu S*, Kawarazaki H*, Muraoka K, Ishizawa K, Yoshida S, Kawarazaki W, Takeuchi M, Ayusawa N, Miyoshi J, Takai Y, Ishikawa A, Shimosawa T, Ando K, Nagase M, Fujita T. (*equal contributor) Rac1 GTPase in rodent kidneys is essential for salt-sensitive hypertension via a mineralocorticoid receptor-dependent pathway. J Clin Invest. 121 (8):3233-3243, 2011 (PMID: 21765214).
Mu S, Shimosawa T, Ogura S, Wang H, Uetake Y, Kawakami-Mori F, Marumo T, Yatomi Y, Geller DS, Tanaka H, Fujita T. Epigenetic modulation of the renal b-adrenergic-WNK4 pathway in salt-sensitive hypertension. Nat Med. 17(5):573–580, 2011 (PMID: 21499270).