Inflammation & Arterial Remodeling:
Novel Mechanisms of Vascular Disease
About Us
My laboratory’s primary focus is understanding the pathophysiology of cardiovascular diseases including atherosclerotic heart disease, the leading cause of death in the United States. My training as a Medical Scientist and Physician Scientist (MSTP), coupled with my clinical expertise as a general cardiologist, has allowed me to lead transformative translational research as an independent researcher.
Specifically, my laboratory conducts experiments investigating mechanisms of atherosclerosis and coronary artery disease (CAD) development through exploring altered inflammatory pathways. We have discovered that biologically active vascular extracellular matrix fragments (termed matrikines) activate CXC Chemokine Receptor 2 (CXCR2), leading to alterations in the structure and function of the vasculature and the heart. Currently, we are studying the mechanisms of matrikine production and proteolytic exosome stimulation as novel mediators of endothelial dysfunction, atherosclerotic disease, and smoke-induced CAD. Our goal is to identify these fragments and exosomes as clinical biomarkers and therapeutic targets of smoke-induced endothelial dysfunction and CAD in populations including military veterans that are disproportionately affected by cardiovascular disease and associated comorbidities.
My laboratory is also an integral component of the UAB Cardiopulmonary Research Program, a multi-disciplinary program that studies the complex interactions between cardiovascular disease and pulmonary diseases. To this end, we are focused on understanding pathophysiology of vascular dysfunction in smoking-induced lung disease, pulmonary hypertension, and comorbid CAD and chronic obstructive pulmonary disease. We assess vascular health through comprehensive physiological, histological, and functional assessments in various model systems to complement mechanistic experiments.
