Andrew Robert Marks

Andrew R. Marks, MD received his undergraduate degree from Amherst College where he was the first student in the history of the college to graduate with honors in two subjects (Biology and English), and his MD from Harvard Medical School. Following an internship and residency in internal medicine at the Massachusetts General Hospital (MGH), he was a post-doctoral fellow in molecular genetics at Harvard Medical School, and then a clinical cardiology fellow at the MGH. He is board certified in internal medicine and in cardiology. Dr. Marks is Chair and Professor of the Physiology and Cellular Biophysics Department at Columbia University. From 2002-2007 Dr. Marks was Editor-in-Chief of the Journal of Clinical Investigation. His honors include: ASCI, AAP, the National Academy of Medicine (2004), American Academy of Arts and Sciences (2005) and the National Academy of Sciences (2005). Doctor of Science Honoris Causa from Amherst College (2009), Docteur Honoris causa, de l’Université de Montpellier (2016), the ASCI Stanley J. Korsmeyer Award (2010), the Pasarow Foundation Award for Cardiovascular Research (2011) and the Ellison Medical Foundation Senior Scholar in Aging Award (2011), Glorney-Raisbeck Award from NY Academy of Medicine (2016). In 2015 Dr. Marks was chosen to present the Ulf von Euler lecture at the Karolinska Institute. Dr. Marks’ identification of the mechanism of action of rapamycin’s inhibition of vascular smooth muscle proliferation and migration lead to the development of the first drug-eluting stent (coated with rapamycin) for treatment of coronary artery disease. This substantially reduced the incidence of in-stent restenosis. In 2014 Dr. Marks reported the high resolution structure of the mammalian type 1 ryanodine receptor/calcium release channel (required for excitation-contraction coupling in skeletal muscle) which he had cloned and worked on since 1989. His research has contributed new understandings of fundamental mechanisms that control muscle contraction, heart function, lymphocyte activation, and cognitive function. He discovered that “leaky” intracellular calcium release channels (ryanodine receptors) contribute to heart failure, fatal cardiac arrhythmias, impaired exercise capacity in muscular dystrophy, post-traumatic stress disorder (PTSD) and Alzheimer’s Disease. Dr. Marks discovered a new class of small molecules (Rycals), developed in his laboratory, that target leaky ryanodine receptor channels and effectively treat cardiac arrhythmias, heart failure, muscular dystrophy and prevent stress induced cognitive dysfunction and symptoms of Alzheimer’s Disease in pre-clinical studies. Rycals are now in clinical trials for the treatment of heart failure and cardiac arrhythmias, and entering clinical trials for the treatment of Duchenne Muscular Dystrophy.