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Rev Endocr Metab Disord. 2008 Dec;9(4):245-54. doi: 10.1007/s11154-008-9100-6.

New insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy.

Author information

1
Departments of Internal Medicine, and Molecular and Integrative Physiology, University of Michigan Medical School, 5520 MSRB1, 1150 W. Medical Center Drive, Ann Arbor, MI, 48109-0680, USA. fbrosius@umich.edu

Abstract

Progression of diabetic nephropathy (DN) is manifested by gradual scarring of both the renal glomerulus and tubulointerstitial region. Over the past several years, the general understanding of the pathogenic factors that lead to renal fibrosis in DN has expanded considerably. In this review, some of the important factors that appear to be involved in driving this fibrosing process are discussed, with special emphasis on newer findings and insights. It is now clear that multiple cell types in the kidney contribute to progressive fibrosis in DN. New concepts about bradykinin, TGF-beta and eNOS signaling as well as JAK/STAT activation and the central role of inflammation in both glomerular and tubulointerstitial fibrosis are discussed.

PMID:
18726161
PMCID:
PMC3776415
DOI:
10.1007/s11154-008-9100-6
[Indexed for MEDLINE]
Free PMC Article

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