Jing (Jason) O. Wu, PhD, FAHA

Assistant Professor, Physiology

I am an early-stage investigator (ESI) with extensive training in vascular biology, immunobiology, and renal physiology. My laboratory focuses on investigating renal hemodynamic mechanisms in hypertension and chronic kidney disease, examining how the vascular-immune interface regulates kidney perfusion and electrolyte handling, and exploring the susceptibility of these processes to genetic polymorphisms, oxidative stress, and environmental toxicants such as per- and polyfluoroalkyl substances (PFAS).

While human exposure to PFAS has been linked to hypertension and renal dysfunction, a causal relationship has not yet been established. Our current research aims to elucidate the mechanistic effects of chronic PFAS exposure on microvascular dysfunction, renal inflammation, glomerulosclerosis, and abnormalities in renal electrolyte transport. By leveraging our expertise in vascular biology and renal physiology, combined with the advanced PFAS analytic chemistry capabilities of the Southwest Environmental Health Sciences Center and the Omics resources of the Program for Translational Multi-Omics, we are uniquely positioned to investigate the role of PFAS toxicity in the development of cardiovascular and kidney diseases.

Degree(s)

2009 MB Preventive Medicine, Peking University Health Science Center
2014 PhD Pharmacology, Vanderbilt University, Nashville TN
2018 Postdoc Hypertension and Vascular Biology, University of Iowa, IA
2019 Postdoc Hypertension, Vascular Biology, and Renal Physiology, Medical College of Wisconsin, WI

Publication Highlights

Drury ER*, Wu J*, Gigliotti JC, Le TH. Sex Differences in Blood Pressure Regulation and Hypertension: Renal, Hemodynamic, and Hormonal Mechanisms. Physiological Reviews. 2024 Jan 1;104(1):199-251. * Co-first authors.

Wu J, Fang S, Lu KT, Kumar G, Reho JJ, Brozoski DT, Otanwa AJ, Hu C, Wackman K, Agbor LN, Grobe JL, Sigmund CD. Endothelial Cullin3 Mutation Impairs Nitric Oxide-Mediated Vasodilation and Causes Salt-induced Hypertension. Function. 2022 Apr 8;3(3):1-18; zqac017.

Wu J*, Agbor LN, Fang S, Mukohda M, Nair AR, Nakagawa P, Avika Sharma, Morgan DA, Grobe JL, Rahmouni K, Weiss RM, Schwartzman ML, McCormick JA, Sigmund CD*. Failure to Vasodilate in Response to Salt Loading Blunts Renal Blood Flow and Causes Salt-Sensitive Hypertension. Cardiovascular Research. 117(1):308-319, 2021. * Corresponding author

Wu J, Saleh MA, Kirabo A, Itani HA, Montaniel KRC, Xiao L, Chen W, Mernaugh RL, Cai H, Berstein KE, Goronzy JJ, Weyand CM, Curci JA, Barbaro NR, Moreno H, Davis SS, Roberts J, Madhur MS, Davies SS, Roberts J II, Harrison DG. Immune activation caused by vascular oxidation promotes fibrosis and hypertension. J Clin Invest. 126(1):50-67, 2016.

Wu J, Thabet S, Kirabo A, Trott DW, Saleh MA, Xiao L, Chen W, Madhur MS, Harrison DG. Inflammation and mechanical stretch promote aortic stiffening in hypertension through activation of p38 mitogen-activated protein kinase. Circulation Research. 114(4):616-25, 2014.

Complete Publication List