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Am J Physiol Endocrinol Metab. 2008 Nov;295(5):E991-9. doi: 10.1152/ajpendo.90452.2008. Epub 2008 Aug 19.

Abnormalities of IGF-I signaling in the pathogenesis of diseases of the bone, brain, and fetoplacental unit in humans.

Author information

1
Department of Emergency and Organ Transplantation, Section of Internal Medicine, Endocrinology, and Metabolic Diseases, University of Bari, Bari, Italy.

Abstract

IGF-I action is essential for the regulation of tissue formation and remodeling, bone growth, prenatal growth, brain development, and muscle metabolism. Cellular effects of IGF-I are mediated through the IGF-I receptor, a transmembrane tyrosine kinase that phosphorylates intracellular substrates, resulting in the activation of multiple intracellular signaling cascades. Dysregulation of IGF-I actions due to impairment in the postreceptor signaling machinery may contribute to multiple diseases in humans. This article will review current information on IGF-I signaling and illustrate recent results demonstrating how impaired IGF-I signaling and action may contribute to the pathogenesis of human diseases, including osteoporosis, neurodegenerative disorders, and reduced fetal growth in utero.

PMID:
18713961
DOI:
10.1152/ajpendo.90452.2008
[Indexed for MEDLINE]
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