Main Content

Jian-Xiong Chen, MD

Office: G325
(601) 984-1731 (office)
(601) 984-2136 (lab)
Fax: (601) 984-1637

Research interests

  • Oxidants and angiogenesis
  • Angiogenic factors gene therapy on diabetic impaired angiogenesis
  • Myocardial regeneration and bone marrow/stem cell differentiation

Current research

The long-term goals of my laboratory research are to understand the pathogenesis and identify the intracellular molecular basis that may contribute to abnormal angiogenesis and regeneration, exacerbation of cardiac dysfunction and heart failure, then, to develop novel therapies that can prevent or reverse these devastating diabetic cardiovascular diseases. Specifically, my laboratory research interesting is focused on:

  • The receptor tyrosine kinase (RTK) angiopoietins/Tie-2 system, prolyl hydroxylases-2 (PHD2), apelin/APJ and Notch signaling interactions in the regulation of vascular smooth muscle maturation, capillary growth and regression, cardiac hypertrophy and heart failure. By using genetic modified angiopoietins-2 (Ang-2) null, Notch3 null, conditional knockout of PHD2 diabetic mice model, myocardial ischemia-induced angiogenesis in vivo and in vitro angiogenesis models, we will define: (1) the molecular mechanisms by which hyperglycemia or diabetes disrupt angiopoietins/Tie-2 system and cause vessel immaturation and regression;
  • Their interactive effects with PHD2/HIF-1a signaling and apelin/APJ on myocardial neovessel maturation and angiogenesis;
  • The mechanisms by which hyperglycemia interferes with pro-inflammatory programme of endothelial cell with a focus on the role of elevated Ang-2;
  • Whether disruption of Jagged1/Notch3 contributes to Ang-2 and diabetes-induced abnormal vascular smooth muscle maturation, vascular progenitor differentiation and facilitate adverse cardiac remodeling and heart failure in diabetes. Identify novel molecular basis as a potential therapeutic target in diabetic cardiac hypertrophy and fibrosis will provide novel approaches to prevent and/or reverse diabetic myocardial ischemia disease.