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(Circulation Research. 2005;97:411.)
© 2005 American Heart Association, Inc.

Editorials

Aging and Longevity

The IGF-1 Enigma

Piero Anversa

From the Cardiovascular Research Institute, Department of Medicine, New York Medical College, Valhalla.

Correspondence to Piero Anversa, MD, Cardiovascular Research Institute, Vosburgh Pavilion, New York Medical College, Valhalla, NY 10595. E-mail piero_anversa@nymc.edu

See related article, pages 418–426

Key Words: IGF-1 • stem cells • skeletal and cardiac muscle regeneration

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

IGF-1 belongs to the insulin family of peptides and acts as a growth factor in many tissues and tumors. Locally acting isoform of IGF-1 targeted to skeletal muscle enhances muscle growth and differentiation, prevents age-related muscle atrophy, and potentiates regeneration after injury.^1,2 Similarly, cardiac restricted expression of IGF-1 increases the formation of ventricular myocytes, attenuates myocyte death, and delays the development of an aging myopathy.^3,4 In the heart, the IGF-1–IGF-1 receptor system induces division of cardiac stem cells (CSCs), upregulates telomerase activity, hinders replicative senescence, and preserves the pool of functionally competent CSCs.^4,5 After muscle injury, IGF-1 promotes the activation, mobilization, and differentiation of satellite cells which, together with the recruitment of bone marrow progenitor cells, contribute to skeletal muscle regeneration in old animals.^1,2 Spontaneous repair of damaged muscle typically occurs in young animals and is severely impaired with age. Importantly, heart failure leads to a catabolic state characterized by a progressive loss in skeletal muscle mass and the appearance of cardiac cachexia in the late stages of the disease. This information formed the basis of the study by Schulze et al⁶ published in the current issue of Circulation Research.

The dramatic problem of skeletal muscle wasting with chronic heart failure has become a common clinical reality. Cardiac decompensation is a disease of the elderly, which has reached endemic proportion with the progressive increase in average lifespan of the population in the Western world.⁷ Unfortunately, muscle atrophy cannot easily be reversed, and the pharmacology is palliative at best. Similarly, . . . [Full Text of this Article]

Related Article:

Transgenic Overexpression of Locally Acting Insulin-Like Growth Factor-1 Inhibits Ubiquitin-Mediated Muscle Atrophy in Chronic Left-Ventricular Dysfunction

P. Christian Schulze, Jennifer Fang, Kimberly A. Kassik, Joe Gannon, Mihaela Cupesi, Cathy MacGillivray, Richard T. Lee, and Nadia Rosenthal
Circ. Res. 2005 97: 418-426. [Abstract] [Full Text] [PDF]

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