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(Hypertension. 2004;43:1164.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Profibrotic Effects of Angiotensin II in the Heart

A Matter of Mediators

From the Area of Cardiovascular Pathophysiology, Centre for Applied Medical Research and University Clinic, School of Medicine, University of Navarra, Pamplona, Spain.

Correspondence to Dr Javier Díez, CIMA-Facultad de Medicina, C/ Irunlarrea 1, 31008 Pamplona, Spain. E-mail jadimar@unav.es

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In response to mechanical and/or metabolic stress the myocardium undergoes structural remodeling involving cardiomyocyte hypertrophy and interstitial and perivascular fibrosis.¹ Cardiomyocyte hypertrophy includes an increase in contractile and embryonic protein content, which appears largely on the activation of transcription of the corresponding cardiac genes that encode these proteins. Myocardial fibrosis is the result of the exaggerated deposition of collagen types I and III fibers as a consequence of the predominance of the synthesis over the degradation of collagen molecules. Myocardial remodeling is accompanied by a progressive decline in cardiac function over time, which underlies the pathogenesis of heart failure in patients with chronic cardiac conditions.²

It is now accepted that a number of systemic and locally expressed factors have key roles in the process of myocardial remodeling.¹ One of these factors is angiotensin II (Ang II). Whereas the role of Ang II in cardiomyocyte hypertrophy is well established,³ emerging experimental and clinical evidence is providing support for the notion that this peptide induces myocardial fibrosis.⁴ Several potential pathways may mediate the profibrotic effects of Ang II on the heart. On the one hand, a number of findings indicate that the interaction of Ang II with the Ang II type-1 (AT₁) receptor located in cardiac fibroblasts results in induction of fibroblast hyperplasia, activation of collagen biosynthetic pathways, and inhibition of collagen degradative pathways.⁵ On the other hand, more recent findings suggest that fibrosis may represent the reparative response to myocardial inflammation induced by Ang II through the interaction with AT₁ . . . [Full Text of this Article]

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