Journal
KIDNEY INTERNATIONAL
Volume 91, Issue 3, Pages 552-560Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.kint.2016.08.025
Keywords
endothelial cells; epithelial cells; fibroblasts; fibrosis; inflammation; interstitium
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Funding
- Department of Veteran's Affairs, Veteran's Health Administration, Office of Research and Development
- Veteran's Affairs Merit Awards [1I01BX002025-01, 1I01BX002196]
- National Institutes of Health [RO1-DK108968-01, R01DK095761, RO1-DK-083187, RO1-DK-075594]
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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.
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