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(Circulation Research. 2008;103:776.)
© 2008 American Heart Association, Inc.

Editorials

Shp Shape

FAKs About Hypertrophy

Kathleen A. Martin, John Hwa

From the Departments of Surgery (Vascular) (K.A.M.), Pharmacology and Toxicology (K.A.M., J.H.), and Medicine (Cardiology) (J.H.), Dartmouth Medical School, Lebanon, NH.

Correspondence to Kathleen A. Martin, Department of Surgery, Dartmouth Medical School, One Medical Center Dr, Lebanon, NH 03756. E-mail kathleen.a.martin@dartmouth.edu

See related article, pages 813–824

Key Words: hypertrophy • Shp2 • FAK • mTOR

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

Despite recent advances in cardiovascular disease prevention and treatment, heart failure remains a major cause of morbidity and mortality in Western countries. Cardiac hypertrophy, an increase in heart weight relative to body weight, can be a beneficial adaptive response, as in the heart of the athlete ("physiological hypertrophy"), but it is clear that distinct forms of pathological hypertrophy (induced by pressure or volume overload) can progress to cardiac failure.^1,2 Cardiac hypertrophy, even in the absence of overt failure, has prognostic significance. Hypertensive patients with echocardiographically determined increases in left ventricular mass and geometry have a higher risk of cardiovascular death.³ This finding has led to intensive investigations into drugs that reduce hypertrophy.⁴ Angiotensin-converting enzyme inhibitors have been shown to reduce hypertrophy,⁴ influence remodeling,⁵ and improve survival.⁶ In recent years, we have progressed in dissecting the molecular signaling mechanisms underlying distinct hypertrophic phenotypes (including physiological, concentric, or eccentric), but it appears that our present understanding reflects only the tip of the iceberg of the complex regulation of remodeling in the heart. A major question that remains is how mechanical (and neurohormonal) stimuli are transduced into molecular signals that drive hypertrophy.

Several recent studies reveal that the tyrosine phosphatase Shp2 (Src homology 2 domain–containing protein tyrosine phosphatase), encoded by the Ptpn11 gene, may be a key player in transducing mechanical signals into the molecular and pathophysiological manifestations of cardiac hypertrophy. In this issue of Circulation Research, Marin et al implicate Shp2 as a critical mediator of stretch-induced cardiomyocyte hypertrophy.⁷ Integrins link . . . [Full Text of this Article]

Related Article:

Shp2 Negatively Regulates Growth in Cardiomyocytes by Controlling Focal Adhesion Kinase/Src and mTOR Pathways

Talita M. Marin, Carolina F.M.Z. Clemente, Aline M. Santos, Paty K. Picardi, Vinícius D.B. Pascoal, Iscia Lopes-Cendes, Mário J.A. Saad, and Kleber G. Franchini
Circ. Res. 2008 103: 813-824. [Abstract] [Full Text] [PDF]

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