title: Local angiotensin II and myocardial fibrosis.
abstract: Tissue repair appears in the infarcted heart at both infarcted and noninfarcted myocardium. Experimental evidence gathered to date indicates that myoFb are the predominant cell responsible for collagen formation at sites of repair in the rat heart and related structures. These phenotypically transformed fibroblast-like cells are not normal residents of ventricular tissue. They appear on day 4 at sites of injury and remain abundant for weeks therefore. MyoFb express type I collagen mRNA and ACE and AT1 receptors. ACE inhibitors or AT1 receptor antagonists attenuate collagen accumulation in both infarcted and noninfarcted myocardium. These findings suggest locally generated AngII may have an autocrine function in regulating myoFb collagen turnover.
authors.affiliation: Department of Internal Medicine, University of Missouri Health Sciences Center, Columbia, USA.
authors.forename: Y
authors.initials: Y
authors.lastname: Sun
mesh_terms: D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D003094:Collagen / Q000378:metabolism; D004719:Endomyocardial Fibrosis / Q000473:pathology / Q000503:physiopathology*; D006321:Heart / Q000502:physiology / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D051381:Rats; D011945:Receptors, Angiotensin / Q000502:physiology; D014945:Wound Healing
chemical_list: D011945:Receptors, Angiotensin; D000804:Angiotensin II; D003094:Collagen; D007703:Peptidyl-Dipeptidase A