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10.1016/j.ebiom.2017.04.011

http://scihub22266oqcxt.onion/10.1016/j.ebiom.2017.04.011
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C5440600!5440600!28434946
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suck abstract from ncbi


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pmid28434946      EBioMedicine 2017 ; 19 (ä): 73-83
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  • Hyperglycemia-induced Renal P2X7 Receptor Activation Enhances Diabetes-related Injury #MMPMID28434946
  • Menzies RI; Booth JW; Mullins JJ; Bailey MA; Tam FW; Norman JT; Unwin RJ
  • EBioMedicine 2017[May]; 19 (ä): 73-83 PMID28434946show ga
  • Diabetes is a leading cause of renal disease. Glomerular mesangial expansion and fibrosis are hallmarks of diabetic nephropathy and this is thought to be promoted by infiltration of circulating macrophages. Monocyte chemoattractant protein-1 (MCP-1) has been shown to attract macrophages in kidney diseases. P2X7 receptors (P2X7R) are highly expressed on macrophages and are essential components of pro-inflammatory signaling in multiple tissues. Here we show that in diabetic patients, renal P2X7R expression is associated with severe mesangial expansion, impaired glomerular filtration (? 40 ml/min/1.73 sq. m.), and increased interstitial fibrosis. P2X7R activation enhanced the release of MCP-1 in human mesangial cells cultured under high glucose conditions. In mice, P2X7R-deficiency prevented glomerular macrophage attraction and collagen IV deposition; however, the more severe interstitial inflammation and fibrosis often seen in human diabetic kidney diseases was not modelled. Finally, we demonstrate that a P2X7R inhibitor (AZ11657312) can reduce renal macrophage accrual following the establishment of hyperglycemia in a model of diabetic nephropathy. Collectively these data suggest that P2X7R activation may contribute to the high prevalence of kidney disease found in diabetics.
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