Zhihua Jiang, MD, PhD

Zhihua Jiang, MD, PhD is an associate professor with the Division of Vascular Surgery in the Department of Surgery at the University of Florida College of Medicine. Dr. Jiang began his career at the University of Florida as a research assistant professor in the Department of surgery in 2006. In 2012, he became an assistant professor with the department and in 2021 received tenure as an associate professor.

Dr. Jiang completed a general surgery residency at the Huaihua People’s First Hospital in China, where he also was a resident fellow. He then received a PhD from Tongji Medical University in China. Following his PhD, Dr. Jiang became a chief resident at Guangxi Medical University. He completed a postdoctoral fellowship in vascular biology at the University of Florida College of Medicine.

He has published several dozens of papers, book chapters and abstracts related to the vascular system and vascular surgery. Dr. Jiang has a passion for teaching future generations of medical professionals, as a teacher and mentor for many postdoctoral fellows, medical residents and undergraduates. He has won many awards including the Excellence Award for Assistant Professors and the Research Career Development Award, both from the University of Florida College of Medicine.

Dr. Jiang’s research interests include danger signals, particularly those triggered by damage associated molecular patterns (DAMPs), dysregulated adaptive immune responses and the impact of cytoskeleton deficiency on cell-signaling.

He is a member of the American Physiological Society, and the American Heart Association where he is also a member of the Peripheral Vascular Disease Council and the Arteriosclerosis, Thrombosis and Vascular Biology Council. Dr. Jiang is an avid researcher and has received a number of grants from the NIH and the Florida Department of Health to research various vascular surgery techniques and vascular disease.

My research projects aim to understand mechanisms that drive initiation and progression of aortic aneurysms and dissections (AADs) and to identify critical cellular and molecular targets that hold promise for further translation to effective therapeutics.

1] Danger signals. Danger signals, particularly those triggered by damage associated molecular patterns (DAMPs), are double-edged swords that may facilitate or impair tissue-repairing processes. To this end, my laboratory focuses specifically on TLR-7 signaling incited by self-RNAs released from stressed or dying cells. Multiple mouse models and human tissue samples are employed to address the context-dependent effects of TLR-7 signaling in the development of AADs.

2] Dysregulated adaptive immune responses. Mounting evidence suggests that the biological outcome of immune injury to an organ depends on local immune cell differentiation. It has been postulated that type 2 immunity, a response primarily driven by Th2, NKT2, and ILC2 cells, may drive structural degeneration in target organs, such as the aorta. In contrast, type 1 immunity may direct cells to undergo hyperplastic responses. Since adaptive immunity is activated in human AADs, our lab is investigating the role of type 2 immunity in AAD development.

3] Impact of cytoskeleton deficiency on cell-signaling. Smooth muscle cells sense changes in the mechano-environment via their cytoskeleton system. They transduce mechano-stress into biochemical signals in order to maintain their mechano-homeostasis. Dysfunction of the cytoskeleton system has been implicated in the development of AADs. Currently, we are investigating risk factors, such as smoking and male gender, that render the aortic wall vulnerable to structural weakening and degeneration via impaired the cytoskeleton dynamics and signaling.