Interstitial Fibrosis in Heart Failure pp 167-180 | Cite as
Renin Angiotensin Aldosterone System and Cardiac Extracellular Matrix
Summary
Macrophage and myofibroblast renin and ACE (recruitable) respectively regulate local concentrations of AngI and AngII involved in tissue repair. De novo generation of AngII modulates expression of TGF-β1 whose autocrine/paracrine properties regulate collagen turnover in heart valve leaflets, an exteriorized portion of the normal extracellular matrix, and at sites of fibrous tissue formation that appear in response to various forms of injury involving diverse tissues. Persistent myofibroblasts and their RAS activity at the infarct site contribute to the progressive fibrosis found at and remote to sites of MI. Activation of the circulating RAAS with sustained elevations in plasma AngII and aldosterone further induce the recruitable form of ACE bound to macrophages and myofibroblasts. Locally produced AngII from this source promotes perivascular fibrosis of intramural vessels of noninfarcted myocardium. At these remote sites, such adverse structural remodeling by fibrous tissue eventuates in ischemic cardiomyopathy, a major etiologic factor involved in the appearance of chronic cardiac failure and which contributes to its progressive nature.
Keywords
Angiotensin Converting Enzyme Unilateral Ureteral Obstruction Renin Expression Infarct Scar Fibrous Tissue FormationPreview
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References
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