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(Circulation. 2007;116:2096-2098.)
© 2007 American Heart Association, Inc.

Editorial

The Transforming Growth Factor-ß/Smad3 Pathway

Coming of Age as a Key Participant in Cardiac Remodeling

David Seo, MD; Joshua M. Hare, MD

From the Division of Cardiology, Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Miami, Fla.

Correspondence to Dr Joshua M. Hare, MD, Chief, Division of Cardiology, Director, Interdisciplinary Stem Cell Institute, University of Miami Miller School of Medicine, Clinical Research Building, Suite 1124, 1120 NW 14th St, Miami, FL 33136. E-mail jhare@med.miami.edu

Key Words: Editorials • inflammation • myocardial infarction • remodeling • Smad3 protein • transforming growth factor-ß

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

Myocardial infarction (MI) is followed by a well-described sequence of events known as postinfarction ventricular remodeling, a process that involves both the infarct scar itself and the residual surviving myocardium.¹ The net results of infarct remodeling are changes in chamber size, function, and geometry. Furthermore, the remodeled ventricle becomes a substrate for both heart failure and sudden cardiac death. The elements of post-MI remodeling include infarct expansion, neurohormonal activation, myocardial hypertrophy, myocardial fibrosis, and cellular apoptosis.

Article p 2127

These are linked physiological responses that attempt to compensate for the sudden decrease in contractility resulting from acute myocardial cell death.² Infarct expansion is the thinning of the infarcted segment from slippage and stretching of myocytes and cell rupture. It is highly influenced by hemodynamic loading conditions.³ The prototypic pathways that participate in post-MI remodeling include the autonomic nervous system and renin-angiotensin-aldosterone system, which may be an attempt to maintain blood pressure and cardiac output.⁴ Over time, however, elevated adrenergic activity may lead to further myocardial cell loss from apoptosis,⁵ and both adrenergic and renin-angiotensin-aldosterone system upregulation have an adverse impact on cardiac hemodynamics. Myocardial hypertrophy, fibrosis, and apoptosis are primarily seen in the noninfarcted regions of the heart, particularly within the peri-infarct zones.^2,6–8 Hypertrophy occurs in response to the increased workload for the surviving myocardiocytes, especially under suboptimal hemodynamic conditions. Myocardial hypertrophy, fibrosis, and apoptosis in the noninfarcted regions are believed to result, in part, from the neurohormonal activation of the sympathetic nervous system, renin-angiotensin-aldosterone system and cytokine cascades. The . . . [Full Text of this Article]

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