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Molecular Pharmacology & Physiology

Molecular Pharmacology and Physiology

Yonggang Ma, PhD

Yonggang Ma, PhD

Assistant Professor, College of Medicine Molecular Pharmacology & Physiology

Contact Info 12901 Bruce B. Downs Blvd., MDC 2529
Tampa FL 33612

Academic Email: yma4@usf.edu

Academic Phone:8139741516

Education

  • PhD, Cardiovascular Pharmacology, Peking Union Medical College, 2010

Interdisciplinary and Emerging Signature Programs

  • Allergy, Immunology & Infectious Disease
  • Cardiovascular Sciences
  • Cellular and Molecular Biology

Research Interests

  • Myocardial infarction (MI)-induced ischemic heart failure is the leading cause of morbidity and mortality in the United States. Our research goals are to reveal the cellular and molecular mechanisms whereby innate and adaptive immunity regulate cardiac repair post-myocardial infarction and to accelerate the development of immunomodulatory agents for the treatment of patients with ischemic heart failure. We use mouse myocardial infarction model to investigate how distinct innate (e.g. neutrophils, macrophages, and eosinophils) and adaptive (T and B lymphocytes) immune cells regulate cardiac wound healing response. Current projects include: 1) T lymphopenia in ischemic heart failure; 2) role of age-associated thymic involution in ischemic heart failure; 3) contribution of the thymus to sex differences following myocardial infarction, and 4) innate immune memory in ischemic heart failure.

Recent Publications

  • Ma Y, Kemp SS, Yang X, Wu MH, Yuan SS Cellular mechanisms underlying the impairment of macrophage efferocytosis Immunol Lett. (254) : 41-53, 2023.
  • Ma Y, Yang X, Villalba N, Chatterjee V, Reynolds A, Spence S, Wu MH, Yuan SY. Circulating lymphocyte trafficking to the bone marrow contributes to lymphopenia in myocardial infarction. American journal of physiology. Heart and circulatory physiology. 322(4) : H622-H635, 2022.
  • Ma Y. Role of Neutrophils in Cardiac Injury and Repair Following Myocardial Infarction. Cells. 10(7) , 2021.
  • Ma Y, Yang X, Chatterjee V, Wu MH, Yuan SY. The Gut-Lung Axis in Systemic Inflammation. Role of Mesenteric Lymph as a Conduit. American journal of respiratory cell and molecular biology. 64(1) : 19-28, 2021.
  • Ma Y, Zabell T, Creasy A, Yang X, Chatterjee V, Villalba N, Kistler EB, Wu MH, Yuan SY. Gut Ischemia Reperfusion Injury Induces Lung Inflammation via Mesenteric Lymph-Mediated Neutrophil Activation. Frontiers in immunology. 11: 586685, 2020.
  • Lindsey ML, Jung M, Yabluchanskiy A, Cannon PL, Iyer RP, Flynn ER, DeLeon-Pennell KY, Valerio FM, Harrison CL, Ripplinger CM, Hall ME, Ma Y. Exogenous CXCL4 infusion inhibits macrophage phagocytosis by limiting CD36 signalling to enhance post-myocardial infarction cardiac dilation and mortality. Cardiovascular research. 115(2) : 395-408, 2019.
  • Ma Y, Mouton AJ, Lindsey ML. Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction. Translational research : the journal of laboratory and clinical medicine. 191: 15-28, 2018.
  • Ma Y, Yabluchanskiy A, Iyer RP, Cannon PL, Flynn ER, Jung M, Henry J, Cates CA, Deleon-Pennell KY, Lindsey ML. Temporal neutrophil polarization following myocardial infarction. Cardiovascular research. 110(1) : 51-61, 2016.
  • Ma Y, Chiao YA, Clark R, Flynn ER, Yabluchanskiy A, Ghasemi O, Zouein F, Lindsey ML, Jin YF. Deriving a cardiac ageing signature to reveal MMP-9-dependent inflammatory signalling in senescence. Cardiovascular research. 106(3) : 421-31, 2015.
  • Ma Y, Halade GV, Zhang J, Ramirez TA, Levin D, Voorhees A, Jin YF, Han HC, Manicone AM, Lindsey ML. Matrix metalloproteinase-28 deletion exacerbates cardiac dysfunction and rupture after myocardial infarction in mice by inhibiting M2 macrophage activation. Circulation research. 112(4) : 675-88, 2013.
  • Ma Y, Chiao YA, Zhang J, Manicone AM, Jin YF, Lindsey ML. Matrix metalloproteinase-28 deletion amplifies inflammatory and extracellular matrix responses to cardiac aging. Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada. 18(1) : 81-90, 2012.