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Cardiovascular Research 2000 46(2):264-268; doi:10.1016/S0008-6363(00)00044-4
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Angiotensin II, adhesion, and cardiac fibrosis

Janet M. Schneea and Willa A. Hsueha,b,*

aUniversity of California—Los Angeles, School of Medicine, Division of Endocrinology, Diabetes, and Hypertension, Warren Hall, 2nd Floor, Rm 24-130, 900 Veteran Avenue, Mail Code 178622, Los Angeles, CA 90024, USA
bMolecular Biology Institute, Los Angeles, CA, USA

* Corresponding author. Tel.: +1-310-794-7555; fax: +1-310-794-7654

Angiotensin II (AII) plays a critical role in cardiac remodeling. This peptide promotes cardiac myocyte hypertrophy and cardiac fibroblast interstitial fibrotic changes associated with left ventricular hypertrophy, post myocardial infarction remodeling and congestive heart failure. AII mediates cardiac myocyte hypertrophy directly via induction of immediate early genes through a MAP kinase dependent pathway. In addition, it mediates cardiac hypertrophy indirectly by stimulating release of norepinephrine from cardiac nerve endings and endothelin from endothelial cells. AII also has multiple effects on cardiac fibroblasts: it induces cardiac fibroblast proliferation, synthesis and secretion of adhesion molecules and extracellular matrix proteins, and expression of integrin adhesion receptors. In addition it stimulates cardiac fibroblasts to adhere more vigorously to defined matrixes. This review will discuss the molecular pathways that have been implicated in these AII induced effects in the cardiac fibroblast.

KEYWORDS Angiotensin; Extracellular matrix; Fibrosis; Hypertrophy


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