AJP - Endo AJP: Advances in Physiology Education
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Endocrinol Metab 295: E991-E999, 2008. First published August 19, 2008; doi:10.1152/ajpendo.90452.2008
0193-1849/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
295/5/E991    most recent
90452.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Laviola, L.
Right arrow Articles by Giorgino, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Laviola, L.
Right arrow Articles by Giorgino, F.

REVIEW

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

Luigi Laviola, Annalisa Natalicchio, Sebastio Perrini, and Francesco Giorgino

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

Submitted 20 May 2008 ; accepted in final form 15 August 2008

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.

insulin-like growth factor I; insulin-like growth factor I receptor; osteoblasts; osteoporosis; neurodegenerative disorders; placenta; intrauterine growth restriction


Address for reprint requests and other correspondence: F. Giorgino, Dept. of Emergency and Organ Transplantation, Section of Internal Medicine, Endocrinology, and Metabolic Diseases, Univ. of Bari, Piazza Giulio Cesare, 11, I-70124 Bari, Italy (e-mail: f.giorgino{at}endo.uniba.it)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.