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

Gewin L, Zent R, Pozzi A
Kidney Int. 2017 91 (3): 552-560

PMID: 27773427 · PMCID: PMC5313325 · DOI:10.1016/j.kint.2016.08.025

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.

Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

MeSH Terms (8)

Animals Cell Communication Cytokines Fibrosis Humans Kidney Renal Insufficiency, Chronic Signal Transduction

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