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(Circulation. 1996;94:2361-2363.)
© 1996 American Heart Association, Inc.

Articles

de Modulatione Cordis

Ralph A. Kelly, MD; Thomas W. Smith, MD

the Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston Mass.

Correspondence to Ralph A. Kelly, Brigham and Women's Hospital, 75 Francis St, Boston MA 02115. E-mail rakelly@bics.bwh.harvard.edu.

Key Words: Editorials • genes • molecular biology • growth substances • hypertrophy • interleukins • signal transduction

	Introduction

 

When I first gave my mind to vivisection, as a means of discovering the motions and uses of the heart, and sought to discover these from actual inspection, and not from the writings of others, I found the task so truly arduous, so full of difficulties, that I was almost tempted to think, with Fracastorius, that the motion of the heart was only to be comprehended by God.—William Harveyde Motu Cordis, 1628As quoted by E.H. Starling in his Linacre Lecture on the Law of the Heart, 1918

The gradual unfolding of our awareness of the Frank-Starling, adrenergic, and cholinergic mechanisms for beat-to-beat regulation of cardiac function from the late 19th century through the 1960s has given way to an explosive growth of knowledge regarding cellular signaling starting with the elucidation of the structure and function of G-protein–coupled receptors and their downstream effectors. To this rapidly evolving picture we can now add a large, complex, and fascinating array of cytokine-activated signaling pathways that mediate the changes in gene expression that underlie long-term adaptation of cardiac form and function.

Recent developments in cell and molecular biology yield a number of important insights into the cellular and subcellular signaling events that direct cardiac morphogenesis during development and myocardial growth and adaptation in the early postnatal and adult heart. These insights have been gained through unexpected, serendipitous observations and results generated by research focusing directly on the identification of previously unidentified cardiac growth-promoting agents. For example, the targeted disruption of the gene for . . . [Full Text of this Article]

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