Abstract | PURPOSE OF REVIEW: RECENT FINDINGS: CCN-2 is upregulated in the clinical and preclinical models of diabetic nephropathy by multiple stimuli, including elevated glucose, advanced glycation, some types of lipid, various hemodynamic factors, as well as hypoxia and oxidative stress. CCN-2 has bioactivities that suggest it may mediate diabetic nephropathy pathogenesis, especially in extracellular matrix accumulation, through both induction of new matrix and inhibition of matrix degradation. CCN-2 also has proinflammatory functions. Moreover, recent studies using antibodies or antisense technologies in animal and early phase clinical trial settings have shown that inhibition of renal CCN-2 expression or action may prevent diabetic nephropathy. Additionally, determination of renal and blood levels of CCN-2 as a marker of diabetic renal disease and its progression appears to have value. SUMMARY: Recent publications implicate CCN-2 as both an evolving marker and mediator of diabetic nephropathy.
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Authors | Susan V McLennan, Maryam Abdollahi, Stephen M Twigg |
Journal | Current opinion in nephrology and hypertension
(Curr Opin Nephrol Hypertens)
Vol. 22
Issue 1
Pg. 85-92
(Jan 2013)
ISSN: 1473-6543 [Electronic] England |
PMID | 23197157
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
- Biomarkers
- Connective Tissue Growth Factor
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Topics |
- Animals
- Biomarkers
(blood)
- Connective Tissue Growth Factor
(blood, metabolism)
- Diabetic Nephropathies
(blood, metabolism)
- Extracellular Matrix
(metabolism)
- Humans
- Up-Regulation
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