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(Circulation. 2003;108:638.)
© 2003 American Heart Association, Inc.

Editorial

Is Nuclear Factor B an Attractive Therapeutic Target for Treating Cardiac Hypertrophy?

Nicole H. Purcell, PhD; Jeffery D. Molkentin, PhD

From the Division of Molecular Cardiovascular Biology, Department of Pediatrics, Children’s Hospital Medical Center, Cincinnati, Ohio.

Correspondence to Jeffery D. Molkentin, PhD, Division of Molecular Cardiovascular Biology, Department of Pediatrics, Children’s Hospital Medical Center, 3333 Burnet Ave, Cincinnati, OH 45229-3039. E-mail jeff.molkentin@chmcc.org

Key Words: Editorials • hypertrophy • apoptosis • heart failure

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

Cardiovascular disease is the leading cause of morbidity and mortality in the United States. In most instances, heart failure is the final consequence of many underlying disease etiologies such as long-standing hypertension, coronary heart disease, valvular insufficiency, arrhythmia, viral myocarditis, and mutations in sarcomere-encoding genes. A compensatory enlargement of the myocardium, or hypertrophy, typically accompanies many of the predisposing insults discussed above and is a leading predictor for the development of more serious and life-threatening disease.^1,2 Given the strong association between the presentation of pathological cardiac hypertrophy and a progressive deterioration in myocardial function, investigators have focused on understanding the molecular mechanisms that initiate the compensatory growth response or that precipitate the transition to heart failure. A number of signal transduction pathways are thought to play pivotal roles in mediating the hypertrophic growth of the myocardium in response to pathological stimuli.³ In this issue of Circulation, Cook et al⁴ focus their attention on the nuclear factor (NF)–B signaling pathway as a potentially important intracellular mediator of cardiac hypertrophy.

See p 664

NF-B is a transcription factor that can directly regulate the expression of immediate-early genes and genes involved in the stress response following a variety of physiological or pathological stimuli. Traditionally, the NF-B pathway has been implicated as a pivotal intracellular mediator of the inflammatory response associated with septic shock, ischemia-reperfusion injury, acute respiratory distress syndrome, viral-induced cytotoxic effects, and cytokine-mediated chronic disease states.⁵ These disease associations have made NF-B an attractive target for pharmacological . . . [Full Text of this Article]

Related Article:

A20 Is Dynamically Regulated in the Heart and Inhibits the Hypertrophic Response

Stuart A. Cook, Mikhail S. Novikov, Youngkeun Ahn, Takashi Matsui, and Anthony Rosenzweig
Circulation 2003 108: 664-667. [Abstract] [Full Text]

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