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(Hypertension. 2007;49:767.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Ionotropic Stress and Integrin

Another Link to Myocardial Remodeling

Saraswati Pokharel; Umesh C. Sharma

From the Hypertension and Vascular Research Division (S.P.), Henry Ford Health System, Detroit, Mich; and the Department of Internal Medicine (U.C.S.), Rosalind Franklin University Medical School, North Chicago, Ill.

Correspondence to Umesh C. Sharma, Department of Internal Medicine, Rosalind Franklin University Medical School, 3333 Green Bay Rd, North Chicago, IL. E-mail umesh.sharma@va.gov

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

Cardiac remodeling is an adaptive response to chronically increased wall stress. Adaptive remodeling of the myocardium, caused either by increased workload or ionotropic stress, requires mediators for the communication of cardiac cells with their surrounding extracellular matrix.¹ Integrins are likely candidates that transduce increased mechanical force into the intracellular biochemical signals. In this issue of Hypertension, Krishnamurthy et al² report a potential role of myocardial ß1-integrin in the adaptive and maladaptive remodeling that occurs in isoproterenol-induced left ventricular hypertrophy. To place the findings of this study in context with emerging studies regarding myocardial remodeling and the progression to left ventricular failure, a brief review of the biology of ß1-integrin with respect to myocardial hypertrophy and remodeling is presented here.

Integrins are heterodimeric cell-surface receptors composed of and ß subunits that function as adhesive and signaling molecules, as well as mechanotransducers.³ In noncardiac cells, it has been demonstrated that integrins respond to abnormal strain in a manner similar to that which would be found during pressure or volume overload in the heart.⁴ Integrins are expressed in various types of cells, including leukocytes, endothelial cells, vascular smooth muscle cells, fibroblasts, and myocytes. Previously, integrins were considered as the structural protein essential for maintaining the integrity of the cell–matrix interaction.³ Emerging studies have established the role of integrins in signal transduction cascades involved in cell migration, proliferation, and growth. ß1-Integrin is a dominant subunit expressed in the heart, which is shown to participate in the hypertrophic response of cardiac ventricular myocytes.⁵

The . . . [Full Text of this Article]

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