The role of IL-18 in type 1 diabetic nephropathy: The problem and future treatment

Cytokine. 2016 May;81:15-22. doi: 10.1016/j.cyto.2016.01.014. Epub 2016 Feb 5.

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: Diabetic nephropathy; IL-18; IL-18 binding protein; Renal complications; Type 1 diabetes mellitus.

Publication types

  • Review

MeSH terms

  • Diabetic Nephropathies / immunology*
  • Diabetic Nephropathies / metabolism
  • Diabetic Nephropathies / prevention & control
  • Forecasting
  • Humans
  • Inflammation / immunology*
  • Inflammation / metabolism
  • Inflammation Mediators / antagonists & inhibitors
  • Inflammation Mediators / immunology*
  • Inflammation Mediators / metabolism
  • Interleukin-18 / antagonists & inhibitors
  • Interleukin-18 / immunology*
  • Interleukin-18 / metabolism
  • Models, Immunological
  • Molecular Targeted Therapy / methods
  • Molecular Targeted Therapy / trends
  • Receptors, Interleukin-18 / immunology
  • Receptors, Interleukin-18 / metabolism
  • Signal Transduction / drug effects
  • Signal Transduction / immunology

Substances

  • Inflammation Mediators
  • Interleukin-18
  • Receptors, Interleukin-18