Dr. D. Gregg Rokosh will be joining the Cardiology Division faculty as of September 2021 as an Associate Professor of Medicine. He earned his BS in 1987 at the University of Saskatchewan and his PhD in 1993 at the same University. He did his postgraduate work at the University of California, San Francisco from 1993 to 2000 before joining the faculty at the University of Louisville in 2000 as an Assistant Professor. He got promoted to an Associate Professor in 2011 at the University of Louisville and then joined the faculty at the University of Alabama as an Associate Professor in 2015. The immune system plays an integral role in many facets of the myocardial injury and dysfunction with increasing complexity of interaction among innate and adaptive responses.
The current focus is on the neutrophils in the context of chronic ischemic injury and heart failure with specific interest in the mechanisms underlying neutrophil activation, in particular, damage associated molecular patterns generated myocardial dysfunction (DAMPs) that interact to generate distinct neutrophil responses. DAMPs are key factors in neutrophil activation that define neutrophil function. DAMPs stimulation of neutrophil NETosis and extracellular trap (NET) generation is an important factor contributing to myocardial dysfunction and adverse remodeling. There is an interest in defining the mechanisms associated with NETotic neutrophil death and how they contribute to the negative impact in heart failure and also in how neutrophil activation affects the functional activation and polarization of other innate and adaptive immune cells and their impact on myocardial dysfunction.
Myocardial DAMPs and effects on deleterious neutrophil functions are key therapeutic targets and we actively pursue these in studies that block or inhibit well defined targets. These studies are critical in translating this novel understanding of neutrophil pathology in heart failure into effect clinical therapies. Key interests: Receptor function and signal transduction in inflammation in cardiovascular disease. Research areas: Current research focuses on the role of damage associated molecular patterns produced by dysfunctional and failing hearts in recruitment of immune cells and their activation contributing to progressive decline in heart function and left ventricle adverse remodeling in heart failure.