Progression of chronic kidney disease: too much cellular talk causes damage

Kidney Int. 2017 Mar;91(3):552-560. doi: 10.1016/j.kint.2016.08.025. Epub 2016 Oct 20.

Abstract

Tubulointerstitial fibrosis, tubular atrophy, and peritubular capillary rarefaction are major hallmarks of chronic kidney disease. The tubulointerstitium consists of multiple cell components including tubular epithelial, mesenchymal (fibroblasts and pericytes), endothelial, and inflammatory cells. Crosstalk among these cell components is a key component in the pathogenesis of this complex disease. After severe or recurrent injury, the renal tubular epithelial cells undergo changes in structure and cell cycle that are accompanied by altered expression and production of cytokines. These cytokines contribute to the initiation of the fibrotic response by favoring activation of fibroblasts, recruitment of inflammatory cells, and loss of endothelial cells. This review focuses on how augmented growth factor and cytokine production induces epithelial crosstalk with cells in the interstitium to promote progressive tubulointerstitial fibrosis after renal injury.

Keywords: endothelial cells; epithelial cells; fibroblasts; fibrosis; inflammation; interstitium.

Publication types

  • Review
  • Research Support, N.I.H., Extramural
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Cell Communication*
  • Cytokines / immunology
  • Cytokines / metabolism*
  • Fibrosis
  • Humans
  • Kidney / immunology
  • Kidney / metabolism*
  • Kidney / pathology
  • Renal Insufficiency, Chronic / immunology
  • Renal Insufficiency, Chronic / metabolism*
  • Renal Insufficiency, Chronic / pathology
  • Signal Transduction*

Substances

  • Cytokines