Mark W. Cunningham
Assistant Professor, Physiology
- BS, Morehouse College, 2008
- PhD, University of Florida School of Medicine, 2014
- MBA, Else School of Management at Millsaps College, 2017
Dr. Mark W. Cunningham Jr. is a native of the Atlanta, Georgia metropolitan area and graduate of Morehouse College. He received his doctoral degree from the University Of Florida College Of Medicine in 2014 from the department of Physiology and Functional Genomics. In 2014 he joined the Department of Pharmacology and Toxicology at the University of Mississippi Medical Center (UMMC) as a post-doctoral fellow. Three years later he was promoted to an instructor; and within a year received the American Heart Association (AHA) Early Career Grant in 2018. After receiving the AHA grant, he was promoted to an Assistant Professor at UMMC where he established his laboratory. Currently he has acquired a new position as assistant professor tenure track at the University of North Texas Health Science Center in Fort Worth, Texas. His research interest examines the mechanisms of cerebrovascular dysfunction, CVD, and hypertension in women (during pregnancy and postpartum) and their offspring. He has an active publishing record (over 42 articles), participates in professional societies, and has attend numerous scientific conferences where he has given oral presentations and been the recipient of several awards. Mark enjoys traveling, learning, reading, mentoring, and community outreach.
My research interest examines the mechanisms (such as inflammation, mitochondrial dysfunction, decreased nitric oxide bioavailability, and increase oxidative stress) of cerebrovascular dysfunction, cardiovascular disease (CVD), and hypertension in women (during pregnancy and postpartum) with hypertensive pregnancy complications and their offspring. Preeclampsia (PE), hypertension during pregnancy, not only affects the mother’s short-term (during pregnancy) and long-term (post-partum) health, but also the health of the neonates into adulthood. Two important factors that are associated with PE are Interleukin 17(IL-17) and the angiotensin II type 1 receptor agonistic autoantibodies (AT1-AA). My current research endeavor is to determine if blockade or interference with IL-17 and/or AT1-AAs during PE can improve maternal and fetal outcomes during pregnancy and later in life. My research areas of expertise include and are not limited to hypertension, women’s health, pregnancy, preeclampsia, and fetal programming.
Hypertension, Pregnancy, Preeclampsia, Fetal Programming, Cerebrovascular Dysfunction, Mitochondria Dysfunction and Oxidative stress, and Cardiovascular Disease
- Test the hypothesis that AT1-AA and/or IL-17 blockade will improve blood pressure, inflammation, oxidative stress, mitochondria function, mitochondrial oxidative stress, cerebrovascular function, and cardiac dysfunction in preeclampsia, by using a preeclamptic rat model of placental ischemia in pregnant rats.
- Test the same hypothesis mentioned above in A) postpartum preeclamptic rats and B) the offspring of preeclamptic rats.
- Identify the sex differences in hypertension, oxidative stress, mitochondria function, mitochondrial oxidative stress, cerebrovascular function, and cardiac dysfunction in the offspring of preeclamptic rats.
- Characterize and examine the hypertensive, cardiovascular, renal, and cerebrovascular dysfunction/pathophysiology of second-generation pregnancies of preeclamptic rats.
- American Heart Association (AHA) Early Career Award -AHA 18CDA34110264
- Renal Physiology Cardiovascular Physiology Endocrine Physiology Hypertension