Main Content

Heng Zeng, MD

Assistant Professor

Office: G754

Lab Room G754

(601) 984-2136 (office)
(601) 984-2136 (lab)
Fax: (601) 984-1637


Research interests

  • Sex difference in the regulation of endothelial metabolic reprogramming and heart failure with preserved ejection fraction (HFpEF)
  • Sex difference in the coronary microvascular dysfunction (CMD) and diastolic dysfunction of aged female.
  • Molecular mechanisms and signaling transduction in vascular stiffness and calcification

Current research

Project 1. Sex difference of endothelial glucose metabolism and coronary microvascular dysfunction in aged female. Cardiovascular disease is the leading cause of death in women. Up to 65% of women with symptoms of myocardial ischemia do not have obstructive coronary artery disease. However, a majority of these woman have shown coronary microvascular dysfunction (CMD) as evidence by a reduction in coronary flow reserve (CFR). Up to date, there is no proven treatments for CMD due to the lack of mechanistic studies. The goal of my research is to elucidate how endothelial glycolysis and its associated metabolic signaling pathways regulate microvascular rarefaction and CMD which may contribute to development of heart failure in aged women.

Project 2. Mechanisms of mitochondrial Sirt3 in vascular remodeling.  Another area of my research interesting is to understand how mitochondrial Sirt3 regulates endothelial/pericyte interactions in vascular hemostasis and vascular remodeling. For the first time, I have revealed a novel role of mitochondrial Sirt3 in sepsis-induced pericyte loss and microvascular dysfunction. I have found that sepsis suppresses Sirt3 expression, which disrupts angiopoietins/Tie-2 signaling pathways; thus leading to a reduction of pericyte/capillary coverage, subsequently promoting vascular leakage, inflammation and end-organ dysfunction in sepsis. We also demonstrated that NG2 pericytes are critical for vascular remodeling during ischemic myocardial repairing and NG2+ cardiac pericyte is promising target for ischemic heart diseases. Specifically, my research is focus on the molecular mechanisms by which endothelial Sirt3 alters pericyte differentiation and vascular stiffness and calcification, which may contribute to hypertension.