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lüll Abnormalities of IGF-I signaling in the pathogenesis of diseases of the bone, brain, and fetoplacental unit in humans Laviola L; Natalicchio A; Perrini S; Giorgino FAm J Physiol Endocrinol Metab 2008[Nov]; 295 (5): E991-9IGF-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.|Bone Diseases/etiology/metabolism/*physiopathology[MESH]|Brain Diseases/etiology/metabolism/*physiopathology[MESH]|Female[MESH]|Fetal Diseases/etiology/metabolism/physiopathology[MESH]|Humans[MESH]|Insulin-Like Growth Factor I/*physiology[MESH]|Placenta Diseases/etiology/metabolism/physiopathology[MESH]|Placenta/metabolism/pathology/physiopathology[MESH]|Pregnancy[MESH]|Signal Transduction/*physiology[MESH] |