Innate Immunity in Diabetic Heart


The mechanisms by which diabetes increases heart failure severity remain poorly understood. Although several processes (such as severity of stenosis, duration of ischemia) contribute to the severity of ischemic injury, recent evidence suggests that infiltration of inflammatory cells plays a critical role not only as a determinant of tissue injury but also in promoting scar formation and infarct healing.

Diabetic and obese mice have higher numbers of circulating Ly6Chigh monocytes and M1 polarized macrophages relative to wild type mice and they display an exaggerated, but relatively ineffective wound healing response.

The overarching goal of my lab is to understand how metabolic changes during diabetes dysregulate the post-MI inflammatory response characterized by excessive recruitment of pro-inflammatory monocytes and delayed resolution of inflammation.

Related Publications


Principal Investigator

Matthew Nystoriak

Marcin Wysoczynski, Ph.D.

Assistant Professor of Medicine

Education

  • Ph.D.: Pomeranian Medical University, Szczecin, Poland

  • M.S.: Jagiellonian University, Krakow, Poland

Research Focus

  • Inflammation and heart failure

  • Cardiac mesenchymal cell biology

  • Exosomes and extracellular vesicles in myocardial repair