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(Circulation Research. 2002;90:833.)
© 2002 American Heart Association, Inc.

Editorials

Exercise, Estrogen, and Ischemic Cardioprotection by Heat Shock Protein 70

Ivor J. Benjamin, Elisabeth Christians

From the Department of Internal Medicine, Molecular Cardiology Research Laboratories, the University of Texas Southwestern Medical Center, Dallas, Tex.

Correspondence to Ivor J. Benjamin, Department of Internal Medicine & Division of Cell and Molecular Biology, UT Southwestern Medical Center, 6000 Harry Hines Blvd, Dallas, TX 75390-8573. E-mail ivor.benjamin@UTSouthwestern.edu

Key Words: estrogen • exercise • sex • ischemia • heat shock proteins

Acute ischemic injury and myocardial infarction arising from coronary artery disease, despite significant strides in medical and surgical management, remain a major public problem. Sex disparity has long been recognized for coronary ischemic events: premenopausal women are at reduced risk for atherosclerotic disease than men of similar age, an advantage that vanishes after menopause.¹ The beneficial effects of estrogen are known to modify vasomotor tone, vascular integrity, blood pressure, lipid profiles, and cholesterol metabolism. However, far less is known about the sex-related effects estrogen has on stress-activated pathways such as the chaperone defense mechanism, which plays fundamental roles in reducing oxidative damage ensuing from myocardial ischemia and reperfusion injury.^2,3

In this issue of Circulation Research, Paroo and coworkers⁴ have addressed the hypothesis that sexual dimorphism in cardiac heat shock protein 70 (Hsp70) expression induced by exercise is modulated by estrogen and that such effects confer sex-specific protection against ischemic injury. These investigators have shown that a single exercise regimen, 30 m/min for 60 minutes, leads to the induction of Hsp70 expression by 2-fold (24 hours) in male but not in female rats. Whereas exercise upregulates Hsp70 expression in ovariectomized female rats, estrogen replacement abrogates similar effects, suggesting that estrogen plays a key role to repress exercise-induced stress response (in a sex-specific manner). Furthermore, a direct causal mechanism by Hsp70 in mediating the recovery of postischemic cardiac function was convincingly shown using antisense oligonucleotides, an approach that had been previously reported to abrogate Hsp70-dependent protection against simulated ischemia in adult . . . [Full Text of this Article]

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