Title : NOD2 promotes renal injury by exacerbating inflammation and podocyte insulin resistance in diabetic nephropathy.

Pub. Date : 2013 Aug

PMID : 23594678






4 Functional Relationships(s)
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Protein Name
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1 In vitro, NOD2 induced proinflammatory response and impaired insulin signaling and insulin-induced glucose uptake in podocytes. Glucose nucleotide-binding oligomerization domain containing 2 Mus musculus
2 Moreover, podocytes treated with high glucose, advanced glycation end-products, tumor necrosis factor-alpha, or transforming growth factor-beta (common detrimental factors in diabetic nephropathy) significantly increased NOD2 expression. Glucose nucleotide-binding oligomerization domain containing 2 Mus musculus
3 Further, knockdown of NOD2 expression attenuated high glucose-induced nephrin downregulation in vitro, supporting an essential role of NOD2 in mediating hyperglycemia-induced podocyte dysfunction. Glucose nucleotide-binding oligomerization domain containing 2 Mus musculus
4 Further, knockdown of NOD2 expression attenuated high glucose-induced nephrin downregulation in vitro, supporting an essential role of NOD2 in mediating hyperglycemia-induced podocyte dysfunction. Glucose nucleotide-binding oligomerization domain containing 2 Mus musculus