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Transcription factors in the pathogenesis of diabetic nephropathy.
Sanchez AP, Sharma K
Kumar Sharma on 3/24/2010
Expert reviews in molecular medicine
Volume : Pages
11 : e13
Approximately a third of patients with diabetes develop diabetic kidney disease,
and diabetes is the leading cause of end-stage renal disease in most developed
countries. Hyperglycaemia is known to activate genes that ultimately lead to
extracellular matrix accumulation, the hallmark of diabetic nephropathy. Several
transcription factors have been implicated in glucose-mediated expression of
genes involved in diabetic nephropathy. This review focuses on the transcription
factors upstream stimulatory factors 1 and 2 (USF1 and 2), activator protein 1
(AP-1), nuclear factor (NF)-kappaB, cAMP-response-element-binding protein
(CREB), nuclear factor of activated T cells (NFAT), and stimulating protein 1
(Sp1). In response to high glucose, several of these transcription factors
regulate the gene encoding the profibrotic cytokine transforming growth factor
beta, as well as genes for a range of other proteins implicated in inflammation
and extracellular matrix turnover, including thrombospondin 1, the chemokine
CCL2, osteopontin, fibronectin, decorin, plasminogen activator inhibitor 1 and
aldose reductase. Identifying the molecular mechanisms by which diabetic
nephropathy occurs has important clinical implications as therapies can then be
tailored to target those at risk. Strategies to specifically target
transcription factor activation and function may be employed to halt the
progression of diabetic nephropathy.
Investigators with authorship
University of California San Diego
Neuropathy & Neurocognition
cAMP responsive element binding protein 1
trans-acting transcription factor 1
secreted phosphoprotein 1
upstream transcription factor 1
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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