Rate My Professor Taixing Cui

Taixing Cui, M.D., Ph.D., FAHA, is a Professor of Medical Pharmacology and Physiology at the University of Missouri School of Medicine and an investigator at the Dalton Cardiovascular Research Center. He earned his M.D. from The Fourth Military Medical University in Xi’an, P.R. China, in 1989, completed residency and served as nephrologist at the General Hospital of Air Force of the People’s Liberation Army in Beijing from 1989 to 1995, and obtained his Ph.D. from Ehime University School of Medicine in Japan in 2001. His career includes assistant professor positions at Ehime University School of Medicine (2001-2003), instructor at Morehouse School of Medicine (2003-2005), assistant professor at the University of Michigan Cardiovascular Center (2006-2007), and at the University of South Carolina School of Medicine from assistant professor (2007-2016) to tenured associate professor (2016-2022), as well as VA Research Investigator (2021-2022).

Dr. Cui's laboratory investigates cardiovascular adaptive responses and maladaptive remodeling through intercellular and interorgan communications using genetic manipulation, fate mapping, physiology analyses, and omics technologies like single-cell RNA sequencing. Research programs focus on cellular sources of vascular lesions, cardiac protein quality control, heart-adipose communications, and cardiovascular mechanotransduction. His interests encompass posttranslational protein modification, super enhancers, cell fate regulation, extracellular microvesicles, and mechanotransduction. Key publications include “Irisin stimulates browning of white adipocytes through mitogen-activated protein kinase p38 MAP kinase and ERK MAP kinase signaling” (Diabetes, 2014), “Nitrolinoleic acid: an endogenous peroxisome proliferator-activated receptor γ ligand” (Proceedings of the National Academy of Sciences, 2005), “Diabetic downregulation of Nrf2 activity via ERK contributes to oxidative stress–induced insulin resistance in cardiac cells in vitro and in vivo” (Diabetes, 2011), “Nrf2-mediated dichotomy in the vascular system: Mechanistic and therapeutic perspective” (Cells, 2022), “Autophagy inhibition enables Nrf2 to exaggerate the progression of diabetic cardiomyopathy in mice” (Diabetes, 2020), and “CYLD exaggerates pressure overload-induced cardiomyopathy via suppressing autolysosome efflux in cardiomyocytes” (Journal of Molecular and Cellular Cardiology, 2020). He holds the distinction of Fellow of the American Heart Association.