Role of the JAK/STAT signaling pathway in diabetic nephropathy.

@article{Marrero2006RoleOT,
  title={Role of the JAK/STAT signaling pathway in diabetic nephropathy.},
  author={Mario B. Marrero and Amy K L Banes-Berceli and David M. Stern and Douglas C Eaton},
  journal={American journal of physiology. Renal physiology},
  year={2006},
  volume={290 4},
  pages={
          F762-8
        }
}
Excessive cellular growth is a major contributor to pathological changes associated with diabetic nephropathy. In particular, high glucose-induced growth of glomerular mesangial cells is a characteristic feature of diabetes-induced renal complications. Glomerular mesangial cells respond to traditional growth factors, although in diabetes this occurs in the context of an environment enriched in both circulating vasoactive mediators and high glucose. For example, the vasoactive peptide ANG II has… 
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This study identifies SOCS1 mimicking as a feasible therapeutic strategy to halt the onset and progression of renal inflammation and fibrosis in diabetic kidney disease.
Vitamin D protects glomerular mesangial cells from high glucose-induced injury by repressing JAK/STAT signaling
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Changes in the intraglomerular hemodynamics, modulated in part by local activation of the renin-angiotensin system, compound the hyperglycemia-induced injury.
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Main topics this review is addressing are biomarkers of oxidative stress in diabetic nephropathy, the sources of reactive oxygen species (mitochondria, NADPH-oxidases, hyperglycemia, and inflammation), and the redox-sensitive signaling networks (protein kinases, transcription factors, and epigenetic regulators).
JAK inhibition and progressive kidney disease
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  • Biology, Medicine
    Current opinion in nephrology and hypertension
  • 2015
TLDR
Activation of the JAK-STAT pathway appears to play a role in the progression of some chronic kidney diseases, and increased expression of the suppressors of cytokine signaling proteins or pharmacologic inhibition of JAK and STAT proteins could play a therapeutic role in multiple Chronic kidney diseases.
Suppressor of Cytokine Signaling-1 Ameliorates Expression of MCP-1 in Diabetic Nephropathy
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It is suggested that SOCS-1 may attenuate renal damage by ameliorating MCP-1 expression and regulation of the phosphorylation of JAK/STAT in diabetic mice.
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Enhanced activation of janus kinase/signal transducers and activators of transcription (JAK/STAT) proteins in both glomerular and tubulointerstitial cells in humans with diabetic nephropathy and in some animal models is studied.
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The authors discuss the mechanisms by which innate immune pathways might contribute to DKD as well as the therapeutic potential of targeting these pathways.
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