Zhihua Jiang

Zhihua Jiang, PhD

Associate Professor

Department: MD-SURGERY-VASCULAR
Business Phone: (352) 294-5689
Business Email: jiangzh@surgery.ufl.edu

About Zhihua Jiang

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.

Accomplishments

Excellence Award for Assistant Professors
2013 · University of Florida
Research Career Development Award
2008 · University of Florida

Teaching Profile

Courses Taught
2015,2020
GMS6683 Fundamentals of Vascular Physiology and Pathology
2018
BME7980 Research for Doctoral Dissertation
2010
IDH4917 Undergrad Research
2022
GMS6012 Human Genetics

Research Profile

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.

Open Researcher and Contributor ID (ORCID)

0000-0001-8057-823X

Publications

2021
Maresin 1 activates LGR6 signaling to inhibit smooth muscle cell activation and attenuate murine abdominal aortic aneurysm formation.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 35(8) [DOI] 10.1096/fj.202100484R. [PMID] 34320253.
2021
Nicotine Exacerbates TAAD Formation Induced by Smooth Muscle-Specific Deletion of the TGF-β Receptor 2
Journal of Immunology Research. 2021:1-17 [DOI] 10.1155/2021/6880036. [PMID] 34646889.
2020
A validated mouse model capable of recapitulating the protective effects of female sex hormones on ascending aortic aneurysms and dissections (AADs)
Physiological Reports. 8(22) [DOI] 10.14814/phy2.14631. [PMID] 33242364.
2019
Cyclophilin A contributes to aortopathy induced by postnatal loss of smooth muscle TGFBR1.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 33(10):11396-11410 [DOI] 10.1096/fj.201900601RR. [PMID] 31311317.
2017
An X-linked Myh11-CreERT2 mouse line resulting from Y to X chromosome-translocation of the Cre allele
genesis. 55(9) [DOI] 10.1002/dvg.23054. [PMID] 28845554.
2017
Hemodynamic Influence on Smooth Muscle Cell Kinetics and Phenotype During Early Vein Graft Adaptation.
Annals of biomedical engineering. 45(3):644-655 [DOI] 10.1007/s10439-016-1725-0. [PMID] 27624660.
2016
Preexisting smooth muscle cells contribute to neointimal cell repopulation at an incidence varying widely among individual lesions.
Surgery. 159(2):602-12 [DOI] 10.1016/j.surg.2015.08.015. [PMID] 26387788.
2016
Smooth muscle cell-specific Tgfbr1 deficiency attenuates neointimal hyperplasia but promotes an undesired vascular phenotype for injured arteries.
Physiological reports. 4(23) [PMID] 27923978.
2016
Smooth muscle cell-specific Tgfbr1 deficiency promotes aortic aneurysm formation by stimulating multiple signaling events.
Scientific reports. 6 [DOI] 10.1038/srep35444. [PMID] 27739498.
2015
Hypertension overrides the protective effect of female hormones on the development of aortic aneurysm secondary to Alk5 deficiency via ERK activation.
American journal of physiology. Heart and circulatory physiology. 308(2):H115-25 [DOI] 10.1152/ajpheart.00521.2014. [PMID] 25398982.
2015
Time and flow-dependent changes in the p27(kip1) gene network drive maladaptive vascular remodeling.
Journal of vascular surgery. 62(5):1296-302.e2 [DOI] 10.1016/j.jvs.2014.05.015. [PMID] 24953896.
2014
Common and distinctive pathogenetic features of arteriovenous malformations in hereditary hemorrhagic telangiectasia 1 and hereditary hemorrhagic telangiectasia 2 animal models–brief report.
Arteriosclerosis, thrombosis, and vascular biology. 34(10):2232-6 [DOI] 10.1161/ATVBAHA.114.303984. [PMID] 25082229.
2014
Flow reversal promotes intimal thickening in vein grafts.
Journal of vascular surgery. 60(2):471-478.e1 [DOI] 10.1016/j.jvs.2013.06.081. [PMID] 24342069.
2013
Rule-based model of vein graft remodeling.
PloS one. 8(3) [DOI] 10.1371/journal.pone.0057822. [PMID] 23533576.
2012
Monocyte chemoattractant protein-1/CCR2 axis promotes vein graft neointimal hyperplasia through its signaling in graft-extrinsic cell populations.
Arteriosclerosis, thrombosis, and vascular biology. 32(10):2418-26 [DOI] 10.1161/ATVBAHA.112.255786. [PMID] 22904274.
2010
The Mismatch Repair System Modulates Curcumin Sensitivity Through Induction of Dna Strand Breaks and Activation of G(2)-M Checkpoint
Molecular Cancer Therapeutics. 9(3):558-568 [DOI] 10.1158/1535-7163.MCT-09-0627. [PMID] 20145018.
2009
Established neointimal hyperplasia in vein grafts expands via TGF-beta-mediated progressive fibrosis.
American journal of physiology. Heart and circulatory physiology. 297(4):H1200-7 [DOI] 10.1152/ajpheart.00268.2009. [PMID] 19617405.
2009
Hemodynamically driven vein graft remodeling: a systems biology approach.
Vascular. 17 Suppl 1(Suppl 1):S2-9 [PMID] 19426605.
2009
Interplay of CCR2 signaling and local shear force determines vein graft neointimal hyperplasia in vivo.
FEBS letters. 583(21):3536-40 [DOI] 10.1016/j.febslet.2009.10.015. [PMID] 19822149.
2008
An experiment-based model of vein graft remodeling induced by shear stress.
Annals of biomedical engineering. 36(7):1083-91 [DOI] 10.1007/s10439-008-9495-y. [PMID] 18415018.
2008
Danger Signaling Dependent Mechanisms in Flow-Induced Arterial Remodeling
Arteriosclerosis Thrombosis and Vascular Biology. 28
2008
Myd88-Dependent Pathway Initiates Neointimal Hyperplasia Development Independently of Tlr4
Circulation. 118
2007
TGF-beta- and CTGF-mediated fibroblast recruitment influences early outward vein graft remodeling.
American journal of physiology. Heart and circulatory physiology. 293(1):H482-8 [PMID] 17369455.
2007
TNF-alpha and shear stress-induced large artery adaptations.
The Journal of surgical research. 141(2):299-305 [PMID] 17574273.
2007
Tumor necrosis factor-alpha and the early vein graft.
Journal of vascular surgery. 45(1):169-76 [PMID] 17210403.
2006
Early differential MMP-2 and -9 dynamics during flow-induced arterial and vein graft adaptations.
The Journal of surgical research. 134(2):327-34 [PMID] 16488440.
2004
A novel vein graft model: adaptation to differential flow environments.
American journal of physiology. Heart and circulatory physiology. 286(1):H240-5 [PMID] 14500133.
2004
Differential expression and activity of matrix metalloproteinases during flow-modulated vein graft remodeling.
Journal of vascular surgery. 39(5):1084-90 [PMID] 15111865.
2004
Impact of IL-1beta on flow-induced outward arterial remodeling.
Surgery. 136(2):478-82 [PMID] 15300218.
2004
Impact of shear stress on early vein graft remodeling: a biomechanical analysis.
Annals of biomedical engineering. 32(11):1484-93 [PMID] 15636109.
2004
Wall shear modulation of cytokines in early vein grafts.
Journal of vascular surgery. 40(2):345-50 [PMID] 15297832.

Grants

Jul 2020 ACTIVE
Immune injury as a driver for the development of ascending aortic aneurysms and dissections
Role: Principal Investigator
Funding: NATL INST OF HLTH NHLBI
Jul 2020 ACTIVE
Novel specialized pro-resolving lipid mediators in resolution of aortic aneurysms and rupture
Role: Co-Investigator
Funding: NATL INST OF HLTH NHLBI
Aug 2019 ACTIVE
Role of RNA-mediated danger signals in regulating TAAD development
Role: Principal Investigator
Funding: NATL INST OF HLTH NHLBI
Mar 2017 – Feb 2021
Mechanisms for tobacco smoke to modulate aortic aneurysm development
Role: Principal Investigator
Funding: FL DEPT OF HLTH BIOMED RES PGM/J&E KING
Jul 2011 – May 2017
The Dichotomy of Akl1 and Alk5 Signaling Pathways in Vascular Response to Injury.
Role: Principal Investigator
Funding: NATL INST OF HLTH NHLBI

Education

Postdoctoral Fellow in Vascular Biology
2001-2003 · University of Florida
Chief Resident
1999-2001 · Guangxi Medical University – China
PhD
1999 · Tongji Medical University – China
Resident Fellow
1992-1994 · Huaihua People’s First Hospital – China
Residency in General Surgery
1987-1992 · Huaihua People’s First Hospital – China
Medical Degree
1987 · Hengyang Medical College – China

Contact Details

Phones:
Business:
(352) 294-5689
Emails:
Addresses:
Business Mailing:
UNIVERSITY OF FLORIDA COLLEGE OF MEDICINE
PO BOX 100128
DIVISION OF VASCULAR SURGERY AND ENDOVASCULA
GAINESVILLE FL 326100128
Business Street:
D124 VA
GAINESVILLE FL 32610