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Circulation. 2002;106:893-895
doi: 10.1161/01.CIR.0000030720.29247.9F
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(Circulation. 2002;106:893.)
© 2002 American Heart Association, Inc.


Editorial

Cardiovascular Disease and Insulin-Like Growth Factor I

Jan Frystyk, MD, PhD; Thomas Ledet, MD, DSc; Niels Møller, MD, DSc; Allan Flyvbjerg, MD, DSc; Hans Ørskov, MD, DSc

From the Institute of Experimental Clinical Research, Aarhus University Hospital, Aarhus, Denmark.

Correspondence to Professor Hans Ørskov, Medical Research Laboratories, Aarhus Kommunehospital, Norrebrogade 44, DK-8000 Aarhus C, Denmark. E-mail hans.orskov@afdm.au.dk


Key Words: Editorials • cardiovascular diseases • atherosclerosis • diabetes mellitus • growth substances


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

The research field of cardiovascular disease in regard to growth hormone (GH) and its mitogenic mediator insulin-like growth factor I (IGF-I) has a long and distinguished history and is still intensively studied. Medline searches reveal that more than 1000 articles have appeared, demonstrating the importance of IGF-I in development of (and for lesions in) the vascular system. Still, mechanisms are insufficiently elucidated. This is obviously partly due to the complexity of the system with formation of IGF-I and its 6 binding proteins (IGFBPs), not only in the liver but also in almost all other organs (including smooth muscle cells), inducing autocrine/paracrine effects via the ubiquitous IGF-I receptor (including vascular endothelium). More than 80% of circulating IGF-I derives from the liver and acts as a true hormone: 99% bound to IGFBPs and 1% in free form, easily transgressing the capillaries.

See p 939

Studies in animals and cell cultures allow for examination of changes in expression of IGF-I and IGFBPs at the site of action, whereas clinical studies like that of Juul et al1 in this issue of Circulation are restricted to analyses of the blood-borne IGF-I system. The overwhelming majority of previous studies point to IGF-I being a mediator of atherosclerotic processes and diabetic vascular lesions. However, during the last 4 years studies have lent support to Juul et al’s results and so indicated that a low serum IGF-I (and high IGFBP-3) is a risk marker for ischemic heart disease (IHD). This is exactly the opposite scenario of that proposed . . . [Full Text of this Article]




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