speaker-info

Dhandapani Kuppuswamy

Dr. Dhandapani Kuppuswamy

Dr. Dhandapani Kuppuswamy is an Associate Professor of Medicine, Cardiology Division at the Medical University of South Carolina (MUSC), Charleston, South Carolina. As a faculty member for the past 24 years at MUSC, he has been studying cellular and molecular mechanisms involved in cardiac hypertrophy that often leads to congestive heart failure. He got his Masters and PhD degrees at the University of Madras, India and moved to US as a postdoctoral fellow in 1984. As a Research Associate at Washington University, St. Louis, he obtained extensive training in cellular signaling involving growth factor receptor tyrosine kinases and demonstrated for the first time that growth factor receptors undergo desensitization. After joining as a faculty at MUSC, he employed much of his
expertise into cardiology on how integrin-mediated tyrosine kinase signaling promotes growth, survival and differentiation of cardiac muscle cells and fibroblasts. Studies from his lab show that β3 integrinmediated signaling mechanisms activate nonreceptor tyrosine kinases that contribute to cardiomyocyte growth and survival on one hand and promote cardiac fibroblast proliferation and extracellular matrix accumulation on the other hand. His recent collaborative studies show very compelling data that ventricular pressure overload in mice can cause increased levels of CD45+ cells (monocyte-derived cells) in the heart that express fibrogenic markers and that treating these mice with the caveolin-1 scaffolding domain (CSD) peptide can suppresses recruitment and differentiation of CD45+ cells into fibrogenic cells, decrease cardiac fibrosis, decrease vascular leakage and myocyte hypertrophy, and improve ventricular function.

In addition to his research work, Dr. Kuppuswamy has served as the advisor for several PhD students and trained many postdoctoral fellows. He is involved in graduate school teaching and serves in many student admission committees.

I will be speaking on

Heart Failure- Potential Cellular and Molecular Targets for Therapy