NOD-like and Toll-like receptors or inflammasomes contribute to kidney disease in a canonical and a non-canonical manner

Kidney Int. 2013 Aug;84(2):225-8. doi: 10.1038/ki.2013.122.

Abstract

Tissue remodeling in kidney disease involves sterile inflammation, because tissue necrosis, in acute kidney injury, produces endogenous agonists to innate pattern recognition receptors that trigger innate immunity. In chronic kidney disease, however, a functional role of such pattern recognition receptors is questionable. Here we summarize and discuss the current evidence on a potential contribution of canonical and non-canonical pattern recognition receptor signaling in chronic kidney disease.

Publication types

  • Comment

MeSH terms

  • Animals
  • Diabetes Mellitus, Experimental / complications*
  • Diabetic Nephropathies / etiology*
  • Female
  • Humans
  • Inflammation Mediators / metabolism*
  • Insulin Resistance*
  • Male
  • Nephritis / etiology*
  • Nod2 Signaling Adaptor Protein / metabolism*
  • Podocytes / metabolism*

Substances

  • Inflammation Mediators
  • NOD2 protein, human
  • Nod2 Signaling Adaptor Protein
  • Nod2 protein, mouse