Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5896762 | Cytokine | 2016 | 8 Pages |
Abstract
Diabetic vascular complication is a leading cause of diabetic nephropathy, a progressive increase in urinary albumin excretion coupled with elevated blood pressure leading to declined glomerular filtration and eventually end stage renal failure. There is growing evidence that activated inflammation is contributing factor to the pathogenesis of diabetic nephropathy. Meanwhile, IL-18, a member of the IL-1 family of inflammatory cytokines, is involved in the development and progression of diabetic nephropathy. However, the benefits derived from the current therapeutics for diabetic nephropathy strategies still provide imperfect protection against renal progression. This imperfection points to the need for newer therapeutic agents that have potential to affect primary mechanisms contributing to the pathogenesis of diabetic nephropathy. Therefore, the recognition of IL-18 as significant pathogenic mediators in diabetic nephropathy leaves open the possibility of new potential therapeutic targets.
Keywords
TNFNIKNFkBVCAM-1IL-18BPIL-18 binding proteinIL-18TLRMCP-1TRAF-6ICAM-1COX-2natural killerMAPKUAEToll-like receptorUrinary albumin excretiontype 1 diabetes mellitusT helper cellsCyclooxygenase-2IRAKsRenal complicationstumor necrosis factor receptor associated factortumor necrosis factornuclear factor kBintracellular adhesion molecule-1vascular cell adhesion molecule-1Diabetic nephropathyNitric oxideMonocyte chemotactic protein-1mitogen-activated protein kinase
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Authors
Nehal M. Elsherbiny, Mohammed M.H. Al-Gayyar,