Assistant Professor
Office: Biomed 1, B306D
Lab: Biomed 1, B331
Phone: 501-686-5514
Email: hzhang2@uams.edu
Education
Ph.D. – Peking University, 2014
Research Interests
Dr. Zhang was recruited from the Department of Laboratory Medicine and Pathology at the University of Washington (UW) in Seattle. He was awarded his doctorate in biophysics from Peking University before embarking on research as a postdoctoral fellow and Instructor at UW.
Dr. Zhang’s research focuses on cardiac dysfunction in the aging heart with an emphasis on the pathogenic role of elevated proton leak from mitochondria. He explores the strategies of restoring mitochondrial function and stem cell therapies to reverse cardiac dysfunction in preclinical models of aging. Dr. Zhang is the principal investigator of an American Heart Association (AHA) Career Development Award and is an AHA study section member. He has more than 30 original publications and has won several national trainee and junior faculty awards.
Research Support
Ongoing
- AHA Career Development Award (Zhang) 4/1/19-3/31/22
Mechanisms of mitochondrial function rejuvenation to restore diastolic dysfunction. - Bronson Foundation Intramural Grant (Zhang) 1/1/22-12/31/22
Human iPSCs differentiated cardiomyocyte senescence.
Completed
- UW CTMR Pilot Grant supported by NIH (Zhang) 11/16/20-2/28/21
Mitochondrial function rejuvenation to restore aged heart muscle dysfunction - Glenn/AFAR Postdoctoral Fellowship for Translational Research on Aging (Zhang) 1/1/18-12/31/18
SS-31 reversal of mitochondrial dysfunction in the aging heart.
Selected Publications
- Zhang H, Alder NN, Wang W, Szeto H, Marcinek DJ, Rabinovitch PS. Reduction of elevated proton leak rejuvenates mitochondria in the aged cardiomyocyte. eLife. 2020; 9: e60827. (Received Editorial Highlights)
- Whitson JA, Bitto A, Zhang H, Sweetwyne MT, Coig R, Bhayana S, Shankland EG, Wang L, Bammler TK, Mills KF, Imai SI, Conley KE, Marcinek DJ, Rabinovitch PS. SS-31 and NMN: Two paths to improve metabolism and function in aged hearts. Aging Cell. 2020; e13213.
- Chiao YA, Zhang H, Sweetwyne M, Whitson J, Ting YS, Basisty N, Pino L, Quarles E, Nguyen NT, Campbell M, Qian W, Merrihew G, Wang L, Yue Y, Duan D, Granzier H, Szeto H, Marcinek DJ, MacCoss MJ, Rabinovitch PS. Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice. eLife. 2020; 9: e55513.
- Hu Q, Zhang H, Cortés NG, Wu D, Wang P, Zhang J, Mattison JA, Smith E, Bettcher LF, Wang M, Lakatta EG, Sheu SS, Wang W. Increased Drp1 acetylation by lipid overload induces cardiomyocyte death and heart dysfunction. Circulation Research. 2020; 126 (4): 456-470.
- Zhang H, Gong G, Wang P, Zhang Z, Kolwicz SC, Rabinovitch PS, Tian R, Wang W. Heart specific knockout of Ndufs4 ameliorates ischemia reperfusion injury. Journal of Molecular and Cellular Cardiology. 2018; 123:38-45.
- Sun CL, Zhang H, Liu M, Wang W, Crowder CM. A screen for protective drugs against delayed hypoxic injury. PLOS ONE. 2017; 12 (4), e0176061.
- Zhang H, Wang P, Bisetto S, Yoon Y, Chen Q, SheuS.S, Wang W. A novel fission-independent role of DRP1 in cardiac mitochondrial respiration. Cardiovascular Research. 2017; 113(2):160-170. (Received Editorial Highlights, Top five downloaded papers of 2017)
- Xu S, Wang P, Zhang H, Gong G, Cortes NG, Zhu W, Yoon Y, Tian R, Wang W. CaMKII induces transient permeability transition through Drp1 phosphorylation at Serine616 during chronic β-AR stimulation. Nature Communications. 2016; 7:13189.
- Wang W, Zhang H, Cheng H. Mitochondrial flashes: from indicator characterization to in vivo imaging. Methods. 2016; 109: 12-20.
- Zhang H, Shang W, Zhang X, Gu J, Wang X, Zheng M, Wang Y, Zhou Z, Cao JM, Ji G, Zhang R, Cheng H. β-Adrenergic stimulated L-type channel Ca2+ entry mediates hypoxia-induced Ca2+ overload in intact heart. Journal of Molecular and Cellular Cardiology. 2013; 65: 51-8.
- Zhang H, Gomez AM, Wang X, Yan Y, Zheng M, Cheng H. ROS regulation of microdomain Ca2+ signaling at the dyads. Cardiovascular Research. 2013; 98(2): 248-58.