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(Circulation Research. 2001;88:978.)
© 2001 American Heart Association, Inc.

Editorial

Death-Defying Pathways Linking Cell Cycle and Apoptosis

Lorrie A. Kirshenbaum

From the Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre and the Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada.

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

Key Words: cardiac myocyte apoptosis • myocardium • cell cycle

	Introduction

 
One of the most intriguing and perplexing issues to impact contemporary cardiology to date is the concept of myocyte regeneration after injury. In contrast to other cells of the body that retain the ability to regenerate throughout life, cardiac muscle cells lose this inherent property soon after birth. Consequently, growth of the neonatal myocardium occurs by myocyte hypertrophy, as manifested by an increase in cell volume and myofibrillar protein content rather than by cell number. The molecular mechanisms that dissociate cardiac growth from hyperplasia remain unknown. This basic biological fact has significant clinical implications for patients, because loss of viable cardiac cells after acute or chronic myocardial injury or during conditions of increased hemodynamic loading, such as those imposed by uncontrolled hypertension, can have detrimental effects on ventricular performance. In these cases, adaptive cellular growth of adjacent myocytes compensates for the cellular loss and impending contractile load to normalize wall stress. However, in some patients, for reasons unknown, these adaptive physiological processes become inadequate and deteriorate into dilatation and overt heart failure. Despite the substantial progress that has been made during the last two decades of cardiac research, heart failure still remains a prominent cause of death in North America. In particular, chronic congestive heart failure represents a major financial and socioeconomic burden, because patients diagnosed with this form of heart disease require costly medical treatments and chronic long-term care.

At the cellular level, defects in contractile proteins and, more recently, loss of cells through an apoptotic process are considered . . . [Full Text of this Article]

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