The physiological and pathophysiological roles of the GH/IGF-axis in the kidney: Lessons from experimental rodent models
The growth hormone (GH)/insulin-like growth factor (IGF) system plays an important role in renal development, growth, function and pathophysiology. IGF-I has been associated with renal/glomerular hypertrophy and compensatory renal growth. Potential effects on glomerular size are of interest, since a...
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Published in: | Growth hormone & IGF research Vol. 14; no. 6; pp. 418 - 430 |
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Main Authors: | , , |
Format: | Journal Article |
Language: | English |
Published: |
Scotland
Elsevier Ltd
01-12-2004
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Subjects: | |
Online Access: | Get full text |
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Summary: | The growth hormone (GH)/insulin-like growth factor (IGF) system plays an important role in renal development, growth, function and pathophysiology. IGF-I has been associated with renal/glomerular hypertrophy and compensatory renal growth. Potential effects on glomerular size are of interest, since an increase in glomerular size may be permissive for the development of glomerulosclerosis. In an effort to abolish the decline of renal function and possibly to restore the renal structure, different approaches have been tested in experimental models of nephropathy, focusing mainly on early renal changes. The involvement of the GH/IGF system in renal pathophysiology has been studied in much detail in the rat. In view of the growing interest in murine physiology, occurring in large part by genetically modified animals, this review examines those aspects of GH, IGFs, their receptors and binding proteins that relate both to mouse kidney physiology and to a number of conditions characterized by pathophysiological renal changes. A deeper understanding of the role of the GH/IGF system in renal dysfunction may stimulate the development of novel therapeutic approaches aiming at preventing or retarding various kidney diseases. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 1096-6374 1532-2238 |
DOI: | 10.1016/j.ghir.2004.06.003 |