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Zhaokang Cheng

Zhaokang Cheng
Associate Professor, Pharmaceutical Sciences 509-358-7741 PBS 341 Spokane


PhD in biochemistry and molecular biology, Nankai University, China, 2008
Bachelor of Science in biological sciences, Nankai University, China, 2003

Fellowships & Additional Training

  • Research assistant professor, Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, 2015-2016
  • Postdoctoral research associate, Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, 2010-2015
  • Certificate in effective mentoring in the research laboratory, University of North Carolina, Chapel Hill, 2013
  • Postdoctoral fellow, Heart Institute, San Diego State University, 2008-2010


Research Interest: Regulation of cell death and survival in the heart.

Heart disease, the leading cause of death in the United States, is frequently associated with cardiac cell death. Understanding the cell death mechanisms could uncover new drug targets for heart protection.

The long-term research goals of the Cheng lab are to identify novel molecules involved in the regulation of cardiac cell death, including apoptosis, necrosis, and autophagy-dependent cell death. We use biochemical, molecular, cellular, genetic, pathophysiological and histological approaches, to study many types of cardiovascular disorders. Specifically, we are interested in cancer treatment-related cardiotoxicity, myocardial infarction, ischemia/reperfusion injury, and cardiac hypertrophy, among others. Our ultimate purpose is to develop new treatments for heart disease.

Selected Publications

Liu Y, Xia P, Chen J, Bandettini WP, Kirschner LS, Stratakis CA, Cheng Z*. PRKAR1A deficiency impedes hypertrophy and reduces heart size. Physiol Rep. 2020 Mar;8(6):e14405. (* corresponding author)

Xia P, Chen J, Liu Y, Fletcher M, Jensen BC, Cheng Z*. Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1. J Biol Chem. 2020 Mar 27;295(13):4265-4276. (* corresponding author)

Dakup PP, Porter KI, Gajula RP, Goel PN, Cheng Z, Gaddameedhi S. The circadian clock protects against ionizing radiation-induced cardiotoxicity. FASEB J. 2020 Feb;34(2):3347-3358.

Xia P, Liu Y, Chen J, Cheng Z*. Cell cycle proteins as key regulators of postmitotic cell death. Yale J Biol Med. 2019 Dec 20;92(4):641-650. (* corresponding author)

Cheng Z*, Combs M, Zhu Q, Xia P, Opheim Z, Parker J, Mack CP, Taylor JM. Genome-wide RNAi screen identifies regulators of cardiomyocyte necrosis. ACS Pharmacol Transl Sci. 2019; 2(5): 361-371. (* corresponding author)

Xia P, Liu Y, Chen J, Coates S, Liu DX, Cheng Z*. Inhibition of cyclin-dependent kinase 2 protects against doxorubicin-induced cardiomyocyte apoptosis and cardiomyopathy. J Biol Chem. 2018 Dec 21;293(51):19672-19685. (* corresponding author)
Featured by: Science Daily, eCancer News, Medical Express, News Medical, Cardiovascular Business, Health Canal, WSU Insider.

Cheng Z, Zhu Q, Dee R, Opheim Z, Mack CP, Cyr DM, Taylor JM. Focal adhesion kinase-mediated phosphorylation of Beclin1 suppresses cardiomyocyte autophagy and initiates hypertrophic growth. J Biol Chem. 2017;292(6):2065-2079.
Featured by: JBC Editors’ Picks, JBC Author Profile.

Xia P, Liu Y, Cheng Z*. Signaling Pathways in Cardiac Myocyte Apoptosis. Biomed Res Int 2016:9583268. (* corresponding author)

Cheng Z, DiMichele LA, Rojas M, Vaziri C, Mack CP, Taylor JM. Focal adhesion kinase antagonizes doxorubicin cardiotoxicity via p21(Cip1.) J Mol Cell Cardiol. 2014;67:1-11.

Cheng Z, DiMichele LA, Hakim ZS, Rojas M, Mack CP, Taylor JM. Targeted focal adhesion kinase activation in cardiomyocytes protects the heart from ischemia/reperfusion injury. Arterioscler Thromb Vasc Biol. 2012;32(4):924-33.

Cheng Z, Sundberg-Smith LJ, Mangiante LE, Sayers RL, Hakim ZS, Musunuri S, Maguire CT, Majesky MW, Zhou Z, Mack CP, Taylor JM. Focal adhesion kinase regulates smooth muscle cell recruitment to the developing vasculature. Arterioscler Thromb Vasc Biol. 2011;31(10):2193-202.

Cheng Z, Völkers M, Din S, Avitabile D, Khan M, Gude N, Mohsin S, Bo T, Truffa S, Alvarez R, Mason M, Fischer KM, Konstandin MH, Zhang XK, Heller Brown J, Sussman MA. Mitochondrial translocation of Nur77 mediates cardiomyocyte apoptosis. Eur Heart J. 2011;32(17):2179-88.

Cheng Z, Ou L, Liu Y, Liu X, Li F, Sun B, Che Y, Kong D, Yu Y, Steinhoff G. Granulocyte colony-stimulating factor exacerbates cardiac fibrosis after myocardial infarction in a rat model of permanent occlusion. Cardiovasc Res. 2008;80(3):425-34.

Cheng Z, Liu X, Ou L, Zhou X, Liu Y, Jia X, Zhang J, Li Y, Kong D. Mobilization of mesenchymal stem cells by granulocyte colony-stimulating factor in rats with acute myocardial infarction. Cardiovasc Drugs Ther. 2008;22(5):363-71.

Cheng Z, Ou L, Zhou X, Li F, Jia X, Zhang Y, Liu X, Li Y, Ward CA, Melo LG, Kong D. Targeted migration of mesenchymal stem cells modified with CXCR4 gene to infarcted myocardium improves cardiac performance. Mol Ther. 2008;16(3):571-9.

View list of publications from PubMed

Teaching Experience

  • PharmSci 579 Principles of Pharmacology, Washington State University, 2019-present
  • PharDSci 499 Special Problems, Washington State University, 2019-present
  • PATH 715 Molecular and Cellular Pathophysiology of Disease: Systemic Pathology, University of North Carolina, Chapel Hill, 2015-2016

Awards & Honors

  • NIH High Priority, Short-Term Project Award (R56), 2019-2020
  • NIH Pathway to Independence (PI) Award (K99/R00), 2014-2019
  • Excellence in Research Presentation Award, University of North Carolina, Chapel Hill, 2013
  • Outstanding Poster Presentation, IVB/MHI 2012 Annual Spring Research Symposium, University of North Carolina, Chapel Hill, 2012
  • American Heart Association Postdoctoral Fellowship Award, 2011-2013
  • Cultural Fellowship for Outstanding PhD Candidates, Nankai University, China, 2007-2008
  • Novo Nordisk / Novozymes Scholarship, 2007

Additional Information

Cheng has received funding support from the National Institutes of Health and the American Heart Association.