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(Circulation. 2007;115:1827-1829.)
© 2007 American Heart Association, Inc.

Editorial

Transgenic Expression of A20 Prevents Cardiac Cell Death and Myocardial Dysfunction After Myocardial Infarction

James Shaw, BSc; Irwin A. Eydelnant, BScEng; Lorrie A. Kirshenbaum, PhD

From the Departments of Physiology (L.A.K.) and Pharmacology & Therapeutics (J.S., L.A.K.), Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba; and the Department of Chemical Engineering (I.A.E.), Faculty of Engineering, McGill University, Montreal, Quebec, Canada.

Correspondence to Dr Lorrie A. Kirshenbaum, Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Room 3016, 351 Taché Avenue, Winnipeg, Manitoba, Canada, R2H 2A6. E-mail lorrie@sbrc.ca

Key Words: Editorials • apoptosis • heart failure • inflammation • ischemia • myocardial infarction • nuclear factor kappa B

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

Notwithstanding the significant advances in cardiovascular medicine over the last 2 decades, cardiovascular disease is responsible for >45% of all deaths in North America and is reaching pandemic proportions worldwide. In particular, heart failure that results from ischemic injury represents a major clinical challenge because individuals diagnosed with this form of heart disease require costly medical treatments and long-term care. Though the exact cellular defects that ultimately contribute to ventricular dysfunction remain unknown, a unifying theme is that functional loss of cardiac myocytes through an apoptotic process contributes to ventricular remodeling and a decline in ventricular performance in patients post–myocardial infarction (MI).

Article p 1885

Historically, the adult myocardium has been viewed as nonproliferative with a limited capacity for de novo myocyte self-renewal after injury.¹ However, the recent discovery of resident cardiac progenitors coupled with the acknowledged ability of adult cardiac myocytes to actively synthesize DNA² has challenged the current dogma. Despite these seminal observations, the infrequency of synthetic events together with the limited numbers of cardiac progenitors appear inadequate to functionally restore ventricular function in patients with heart failure after MI. Given that cardiac output is directly influenced by the number of functional cardiac myocytes, the ultimate therapeutic goal in the reduction of morbidity and mortality in patients with heart failure post-MI would be to preserve the number of existing myocytes by suppression of the cell death process.³ For this reason, there has been considerable effort to decipher the signaling pathways and cellular factors that govern cell survival mechanisms . . . [Full Text of this Article]