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(Circulation. 2006;113:2032-2034.)
© 2006 American Heart Association, Inc.

Editorial

Akt Signaling and Growth of the Heart

Kenneth Walsh, PhD

From the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, Mass.

Correspondence to Dr Kenneth Walsh, Whitaker Cardiovascular Institute, Boston University School of Medicine, 715 Albany St, W-W-527, Boston, MA 02118. E-mail kxwalsh@bu.edu

Key Words: Editorials • hypertrophy • signal transduction

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

Physiological and pathological stimuli produce clinically and molecularly distinct forms of cardiac growth. Physiological cardiac growth is a feature of normal postnatal development in which an increase in cardiac muscle cell diameter is observed as infants mature to adults.¹ This nonpathological heart growth, sometimes referred to as physiological hypertrophy,² is similar to the growth observed in the hearts of trained athletes in whom the adaptation to increased workload leads to increased vascularization of the myocardium and more forceful ejection.^1,3 In contrast, pathological hypertrophy occurs in patients with hypertension or valvular heart disease. A number of molecular distinctions can be made between physiological and pathological cardiac hypertrophy. For example, pathological cardiac hypertrophy is associated with interstitial fibrosis, activation of a fetal gene program, and myocyte apoptosis, whereas physiological cardiac growth does not display these features. Most studies have focused on elucidating mechanisms of pathological heart growth, whereas the molecular regulation of physiological cardiac growth is less understood. In this issue of Circulation, an article by DeBosch et al⁴ sheds light on the role of Akt1 signaling in the promotion of physiological growth and inhibition of pathological hypertrophy.

Article p 2097

The Akt (also referred to as protein kinase B) family of serine/threonine protein kinases is highly conserved in evolution.⁵ Akt1 and Akt2 share extensive sequence homology at the amino acid level, whereas Akt3 is slightly more divergent in structure and is expressed as a splice variant that lacks a regulatory phosphorylation site.⁶ Akt protein kinases are stimulated by a number . . . [Full Text of this Article]

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