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(Circulation Research. 2004;94:411.)
© 2004 American Heart Association, Inc.

Editorials

Cardiac Stem Cells Fail With Aging

A New Mechanism for the Age-Dependent Decline in Cardiac Function

Maurizio C. Capogrossi

From the Laboratorio di Patologia Vascolare, Istituto Dermopatico dell’Immacolata, Istituto di Ricovero e Cura a Carattere Scientifico, Rome, Italy.

Correspondence to Maurizio C. Capogrossi, MD, Laboratorio di Patologia Vascolare, Istituto Dermopatico dell’Immacolata-IRCCS, Via dei Monti di Creta 104, 00167 Rome, Italy. E-mail capogrossi@idi.it

Key Words: stem cells • aging • heart • oxidative stress • p66^shc

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

Aging, even in apparently healthy individuals without overt cardiovascular disease, is associated with changes in heart structure and compromised cardiac reserve function.¹ These changes per se do not lead to clinical heart failure; however, they make the heart more vulnerable to myocardial ischemia, systemic arterial hypertension, and other pathological conditions, thereby playing a major role in the markedly increased prevalence of heart failure in the elderly. Some of the mechanisms responsible for cardiac aging have been characterized both in humans and in animal models.^2,3 Intimal thickening, enhanced arterial stiffness, and endothelial dysfunction target the arterial wall and, in due time, will have a negative effect on the structure and function of the heart. In addition, old myocardial cells are fewer and larger than those from younger hearts and exhibit a prolonged action potential and contraction duration, a diminished response to ß-adrenergic stimulation, as well as other functional changes. The basic mechanism(s) that underlie cellular aging have not been conclusively established, but oxidative stress may be a key causal element.⁴ The study by Torella et al,⁵ in this issue of Circulation Research, evaluated several markers of myocardial cell aging both in wild-type (WT) and insulin-like growth factor-1 (IGF-1) transgenic (TG) mice. Expression of these markers increased with age and was markedly attenuated in IGF-1 TG animals. Importantly, the study also evaluated the effect of aging on cardiac stem cells (CSCs). Similarly to what occurs in other organs, stem cells are also present in the heart.^6–8 In a pivotal work from . . . [Full Text of this Article]

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