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About Ronald
Ronald Vagnozzi, PhD, serves as Assistant Professor in the Department of Medicine, Division of Cardiology at the University of Colorado Anschutz Medical Campus. He directs the Vagnozzi Lab, dedicated to elucidating cellular mechanisms of injury and stress responses in the heart. The lab focuses on the innate immune system's role in modulating inflammation's effects on wound healing, fibrosis, and tissue remodeling, delineating pathways that promote beneficial repair from those leading to pathological outcomes. Employing mouse models, the team utilizes genetic lineage tracing, gene function studies, signaling pathway analyses, and genome-wide screening to identify regulators of cardiac wound healing and pioneer therapeutic approaches for repairing or rejuvenating damaged hearts. Key research areas include functions of tissue-resident macrophage subsets in cardiac health and disease, damage-sensing signaling pathways, immune cell-fibroblast-extracellular matrix crosstalk, and discovery platforms for novel interventions.
Affiliated with the Gates Institute and the Consortium for Fibrosis Research and Translation (CFReT), Vagnozzi has made significant contributions to cardiovascular research. His high-impact publications encompass 'An acute immune response underlies the benefit of cardiac stem cell therapy' (Nature, 2020), 'Fibroblast-specific TGF-β–Smad2/3 signaling underlies cardiac fibrosis' (Journal of Clinical Investigation, 2017), 'Specialized fibroblast differentiated states underlie scar formation in the infarcted mouse heart' (Journal of Clinical Investigation, 2018), 'c-kit+ cells minimally contribute cardiomyocytes to the heart' (Nature, 2014), and 'The mitochondrial calcium uniporter selectively matches metabolic output to acute contractile stress in the heart' (Cell Reports, 2015). These works, amassing over 6,900 citations, have shaped understanding of immune-fibrotic mechanisms in heart disease. Vagnozzi holds positions on the editorial board of the American Journal of Physiology-Heart and Circulatory Physiology and has received Early Career Research Support from the American Heart Association.
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