Jing Wu

I was trained in vascular biology and immunology in hypertension research. My laboratory investigates the roles of PPARγ (peroxisome proliferator activated receptor γ) and its downstream signaling in renal physiology, immunobiology, and cardiometabolic diseases. Loss-of function mutations in PPARγ (P467L, V290M, etc) cause severe early onset hypertension in humans, while global PPARγ activation reduces blood pressure in multiple clinical trials/studies. We and others have provided compelling evidence that the cardiovascular benefits of global PPARγ activation are mediated by its actions in vascular and immune cells. 

My current K01 award (2021-2025) aims to understand the roles of vascular PPARγ in renal physiology and salt sensitive hypertension. Using the inducible cre-loxP system, we created transgenic mice carrying human hypertension-causing mutations in PPARγ selectively in vascular smooth muscle (S-P467L), which in response to salt loading develop impaired renal perfusion and enhanced sodium retention that ultimately leads to salt sensitive hypertension. These model systems are valuable tools to understand the renal hemodynamic mechanisms of salt sensitivity of blood pressure, the ability of the vascular-tubular interface to regulate renal electrolyte handling, and the vulnerability of these processes to genetic polymorphisms, oxidative stress, and inflammation. 

A second area of interest is to understand T cell PPARγ and Cullin3 in hypertension and metabolic disorders. We have generated mouse models with genetic modifications in PPARγ and Cullin3 selectively in T lymphocytes, which exhibit exaggerated hypertension, target organ damage, and altered adiposity/glucose homeostasis. The goal of this project is to elucidate immune mechanisms of hypertension and the ability of the immune cells to regulate the function of metabolic organs (pancreas, liver, adipose tissue). 

I am committed to promoting innovative, collaborative, inclusive academic research and to mentoring young members of the research team. My ultimate career goal is to apply our findings to translational research that may lead to the development of novel therapies for cardiovascular, renal, and metabolic diseases.

Publications

A complete list of my published work is available at NCBI MyBibliography.

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