A professor of Medicine, Physiology, and Pharmacology and Experimental Therapeutics, Dr. Cohen is the Jay and Louise Coffman Professor of Medicine and Director of the Vascular Biology Unit. Dr. Cohen is also the Co-principal Investigator of the Boston University Cardiovascular Proteomics Center. Dr. Cohen is also a recipient of an R37 MERIT award from the NHLBI and is currently the PI or Co-PI of 6 NIH investigator initiated research studies. In 2008 he was named to a 5 year Robert Dawson Evans Scholar Award by the Department of Medicine. He is a former recipient of the American Heart Association Clinician Investigator and the Established Investigator awards. He is past president of the American Federation for Medical Research and founding president of the American Federation for Medical Research Foundation. Dr. Cohen is distinguished by his elections to the American Society for Clinical Investigation and the Association of American Physicians. He is an elected Fellow of the Cardiovascular Section of the American Physiological Society. He is a member of the editorial boards of the American Journal of Physiology: Heart and Circulatory Physiology and Arteriosclerosis, Thrombosis, and Vascular Biology, and Free Radical Biology and Medicine. Dr. Cohen is a past member of the NIH Experimental Cardiovascular Study Section and currently serves as an ad hoc reviewer for several NIH review groups. The research in the Vascular Biology Unit which Dr. Cohen directs focuses on the effect of vascular and metabolic disease on the function of blood vessels with special emphasis on the role of endothelium-derived nitric oxide and reactive oxygen species. The roles of redox-mediated post-translational protein modifications of cardiovascular proteins including the sarcoplasmic reticulum calcium ATPase, sirtuin-1, and p21ras in cell signaling and disease are a current focus. Applications of these basic areas are currently bein g pursued in funded programs with respect to clinical areas problems of atherosclerosis, impaired ischemia-induced angiogenesis, arterial stiffness, hypertension, and failure of hemodialysis fistulae.

The Vascular Biology Unit led by Dr. Richard Cohen seeks to understand mechanisms of abnormal vascular function and disease in order to better develop therapies. The role of reactive oxygen and nitrogen species is of key importance to that understanding. His group has found that in diabetes, hypertension, and atherosclerosis, the vasodilator, nitric oxide, reacts with superoxide anion, an oxidant produced in diseased blood vessels. As a result of this reaction even more potent oxidants, including peroxynitrite, are formed. Low levels of oxidants form protein cysteine thiol adducts with the low molecular weight antioxidant glutathione. Targeted proteins include the sarcoplasmic reticulum calcium ATPase, p21ras, and sirtuin-1, whose function is thereby altered, consequently modulating cell calcium and signaling. High levels of peroxynitrite can be blamed for inactivating these and other important proteins, such as endothelial nitric oxide synthase and manganese superoxide dismutase. As part of the BU Cardiovascular Proteomics Center, Dr. Cohen and his group are identifying chemical modifications of proteins formed by oxidants with mass spectrometric and protein tagging strategies. These modifications may serve as biomarkers for abnormal tissue and cell signaling as well as abnormal cell function in disease. Such markers have been discovered in diseased human arteries and platelets. A new program focuses on arterial stiffness and hypertension associated with obesity and metabolic disease.