Nikolaos G. Frangogiannis, MD, is the Edmond J. Safra/Republic National Bank of New York Professor of Cardiovascular Medicine at the Albert Einstein College of Medicine in the Bronx. Frangogiannis graduated from the University of Athens School of Medicine in 1990 and two years later left his native Greece to pursue a residency in Internal Medicine at Baylor College of Medicine in Houston. Accepted into the Clinical Investigator Pathway, he got his first research experience in the laboratory of Mark L. Entman, MD, working with a strong group of investigators exploring myocardial inflammation in response to injury. Frangogiannis remained in Houston for 18 years, joining the faculty and establishing an independent laboratory in 1999 to expand on previous concepts on the role of inflammation in cardiac injury and repair, by probing numerous signaling pathways. The laboratory investigated whether the chemokine monocyte chemoattractant protein (MCP)-1/CCL2 was a critical regulator of myocardial infarct healing, using MCP-1 knockout mice to show that the absence of MCP-1 results in attenuated postinfarction left ventricular remodeling, but at the high cost of a prolonged inflammatory phase and delayed replacement of injured cardiomyocytes with granulation tissue.1 Using a closed-chest model of coronary infarction/reperfusion in mice, Frangogiannis’ laboratory discovered that transforming growth factor (TGF)-β/Smad3 signaling, while having antiproliferative effects, actually promotes fibrogenic actions, particularly in the infarct border zone and in the adjacent remodeling myocardium following infarction, expanding the fibrotic process into noninfarcted areas and contributing to diastolic dysfunction.2 In 2010, Frangogiannis moved to New York, where he has deployed new tools to study the cell biology of cardiac remodeling in vivo, whether following infarction or in response to other injurious stimuli, such as metabolic disease. For example, in 2013 his laboratory demonstrated that the matricellular protein thrombospondin-1 has both direct and indirect effects on the cardiac …
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