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(Circulation Research. 1999;85:880.)
© 1999 American Heart Association, Inc.

Editorials

Apoptosis

Rekindling the Mitochondrial Fire

Brian O’Rourke

From The Johns Hopkins University, Department of Medicine, Section of Molecular and Cellular Cardiology, Baltimore, Md.

Correspondence to Brian O’Rourke, PhD, Johns Hopkins University, Section of Molecular and Cellular Cardiology, 720 Rutland Ave, 844 Ross Bldg, Baltimore, MD 21205. E-mail bor@jhmi.edu

Key Words: myocyte • apoptosis • oxidative stress • Bcl-2 • mitochondria

	Introduction

 
An explosion of information has recently emerged highlighting the role of mitochondria in the life and death of cells. The function of mitochondria as the arbiters of a complex signaling cascade urging the cell to its own orchestrated demise is one of a number of new findings fueling a renewed interest in this essential organelle. Perhaps in no other tissue is it more important to maintain mitochondrial function and prevent cell dropout than in cardiac muscle. Pump function quickly fails when the constant high-energy demand of contraction is not met by the efficient generation of ATP through mitochondrial oxidative phosphorylation, and if cell death is triggered in the adult heart, regardless of whether it is through necrotic or apoptotic pathways, there is no way to regenerate lost myocytes.

	Slow Cardiac Death

 
It is perhaps not surprising then to learn that the genetic program during the later stages of development tips the balance of proteins in favor of preventing apoptosis. In this issue of Circulation Research, Cook et al¹ examine the distribution of Bcl-2 family proteins in the rat heart and probe the mechanism of apoptotic cell death by studying H₂O₂-induced cell death in cultured neonatal myocytes. Interestingly, expression of the antiapoptotic proteins Bcl-2 and Bcl-xL was maintained at high levels throughout development to adulthood whereas the proapoptotic proteins Bad and Bax dropped to undetectable levels in the adult heart. In a similar vein, it has been previously shown that Bcl-2 mRNA is high in fetal rat, drops significantly postnatally, and . . . [Full Text of this Article]

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