Mark L. Entman, M.D.
Mark L. Entman, M.D., is chief of Cardiovascular Sciences at Baylor College of Medicine and professor of Medicine, Biochemistry, and Pathology. He is also principal investigator and scientific director of the DeBakey Heart Center at Baylor College of Medicine and The Methodist Hospital.
Dr. Entman is a graduate of Duke University School of Medicine and received his internal medicine and cardiology training at Johns Hopkins and Duke. After completion of his clinical training, he enrolled in the Research Training Program at Duke University where he did graduate work in biochemistry and cell biology. After two years of research at the Armed Forces Institute of Pathology and the National Heart and Lung Institute, Dr. Entman was recruited to Baylor College of Medicine as an assistant professor in 1970. He was a Howard Hughes Medical Investigator from 1971 and 1979 when he assumed his present position. In 1977, Dr. Entman became the chief of the Division of Cardiovascular Sciences and director of the Division of Research of NHLBI National Research and Demonstration Center at Baylor College of Medicine and The Methodist Hospital. In 1985, the DeBakey Heart Center replaced that program and Dr. Entman remained as a research director of the DeBakey Heart Center until recent years. In 1997, Dr. Entman became the scientific director and principal investigator of DeBakey Heart Center; he is also the William J. Osher Professor of Cardiovascular Research.
Dr. Entman's early research interests relate to control of myocardial calcium and sarcoplasmic reticulum function. These studies were continuously supported by the National Heart, Lung and Blood Institutes since before his arrival at Baylor. For this work, Dr. Entman received the Outstanding Research Award from the International Society of Heart Research (1986) and was awarded an NIH MERIT AWARD (1989-1999).
Dr. Entman's other research interests relate to injury in the myocardium. These studies have been supported since 1974 by an RO1 and subsequent Program Project Grants and RO1's. Early studies related to the effects of ischemia and reperfusion on the function of cardiac organelles. In recent years, studies have concentrated on the role of inflammation in cardiac injury following reperfusion of the infarcted myocardium. Studies are aimed at characterizing the accelerated reperfusion-induced inflammation and its role in extending myocardial injury. Dr. Entman and his colleagues have demonstrated the induction of ICAM-1 on viable cardiac myocytes in the jeopardized border zone of a reperfused myocardial infarction. They demonstrated in vivo that the presence of ICAM-1 sensitizes myocardial cells to adhesion-dependent neutrophil induced injury and that ICAM-1 induction during reperfusion results from stimulation by interleukin-6. The work deals with characterizing the cytokine cascade responsible for inflammatory injury of the surviving border zone. Factors influencing both the cardiac and leukocyte response are studied. Paradoxically, reperfusion-induced inflammation also positively influences tissue repair. The overall strategy has been identification of cellular and molecular events that result in injury and identification of potential factors which might reduce inflammatory injury or promote repair. This work has led to investigations of the cellular and molecular link between inflammation and adverse remodeling in the heart. The laboratory has defined, in both murine models and clinical material taken from ischemic cardiomyopathy (in the absence of infarction) the presence of CD45+ fibroblasts. Our studies have demonstrated that these fibroblasts arise from a subset of monocytes attracted to the ventricle through chemokine dysregulation. This population of fibroblasts is not involved in cardiac scar formation after infarction and current study examine the pertinence of this mechanism to cardiac adverse remodeling of other origin. Related studies in the laboratory involve investigation into the cellular and molecular mechanisms involved in myocyte-fibroblast transition. In addition to the requirement for chemokines, our studies suggest that transendothelial migration is necessary for this transition and that the transition is modulated by Fcγ receptor ligands.
Dr. Entman is a member of the American Society for Clinical Investigation and the Association of American Physicians. He received the Distinguished Alumnus Award from Duke University Medical Center in 1996. In 2007, Dr. Entman received the Bowman Award for Outstanding Research from the Institute of Cardiovascular Sciences for his work on the cellular mechanisms of cardiac remodeling and repair. He has also been active in peer review. He was a member of the Pharmacology Study Section of NIH, a member and chairman of the American Heart Association Cardiovascular B Research Study Committee, and a member of the National Cardiology Merit Review Board of the Veteran's Administration, as well as many ad hoc groups. Dr. Entman also served on the Research and Program Evaluation Committee of the American Heart Association and was chairman of the American Heart Association Research Policy Subcommittee. He serves or has served on the editorial boards of all of the major journals associated with cardiovascular research. He has also been the associate editor for Federation Proceedings and FASEB Journal and associate editor of Circulation.