Fibrosis and hypertensive heart disease.
The normal myocardium is composed of a variety of cells: cardiac myocytes and noncardiomyocytes, which include endothelial and vascular smooth muscle cells and fibroblasts. Hypertensive heart disease involves a structural remodeling of muscular and nonmuscular compartments. It is not the quantity but rather the quality of myocardium that accounts for pathologic hypertrophy and predisposes to ventricular dysfunction and arrhythmias, which, in turn, confer increased risk of adverse cardiovascular events. Herein, factors regulating growth of these compartments are reviewed and in particular signals involved in promoting adverse remodeling of intramyocardial coronary arteries and arterioles by fibrous tissue.
Weber
K T
KT
Department of Medicine, University of Tennessee Health Science Center, Memphis 38163, USA. ktweber@utmem.edu
D000818:Animals; D006332:Cardiomegaly / Q000209:etiology* / Q000378:metabolism; D002455:Cell Division; D003331:Coronary Vessels / Q000378:metabolism; D004719:Endomyocardial Fibrosis / Q000209:etiology* / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism; D006131:Growth Inhibitors / Q000378:metabolism; D006133:Growth Substances / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D008955:Models, Cardiovascular; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D012084:Renin-Angiotensin System; D016212:Transforming Growth Factor beta / Q000378:metabolism
D006131:Growth Inhibitors; D006133:Growth Substances; D016212:Transforming Growth Factor beta; D009569:Nitric Oxide