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

Leslie Gewin, Roy Zent, Ambra Pozzi

Research output: Contribution to journalShort surveypeer-review

82 Scopus citations

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.

Original languageEnglish
Pages (from-to)552-560
Number of pages9
JournalKidney International
Volume91
Issue number3
DOIs
StatePublished - Mar 1 2017

Keywords

  • endothelial cells
  • epithelial cells
  • fibroblasts
  • fibrosis
  • inflammation
  • interstitium

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