Genetic approaches to disease and regeneration.
Cardiovascular disease is largely a consequence of coronary artery blockage through excessive proliferation of smooth muscle cells. It in turn leads to myocardial infarction and permanent and functionally devastating tissue damage to the heart wall. Our studies have revealed that elastin is a primary player in maintaining vascular smooth muscle cells in their dormant state and thus may be a useful therapeutic in vascular disease. By studying zebrafish, which unlike humans, can repair damage to heart muscle, we have begun to uncover some of the genes that seem necessary to undertake the de-differentiation steps that currently fail and prevent the formation of new proliferating cardiomyocytes at the site of damage in a mammalian heart.
Department of Cell Biology, Harvard Medical School, Enders 1261, 320 Londwood Avenue, Boston, MA 02115, USA. mkeating@enders.tch.harvard.edu
Mark T
MT
Keating
D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000628:therapy; D002454:Cell Differentiation / Q000502:physiology; D003331:Coronary Vessels / Q000378:metabolism; D004195:Disease Models, Animal; D004549:Elastin / Q000172:deficiency / Q000378:metabolism* / Q000627:therapeutic use; D006321:Heart / Q000502:physiology*; D006801:Humans; D009130:Muscle, Smooth / Q000378:metabolism*; D012038:Regeneration / Q000235:genetics* / Q000502:physiology*; D015027:Zebrafish
D004549:Elastin