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

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

Author information

1
Division of Nephrology, Department of Medicine, Vanderbilt Medical Center, Nashville, Tennessee, USA; Department of Cell and Developmental Biology, Vanderbilt Medical Center, Nashville, Tennessee, USA; Veterans Affairs Medical Center, Nashville, Tennessee, USA.
2
Division of Nephrology, Department of Medicine, Vanderbilt Medical Center, Nashville, Tennessee, USA; Department of Cell and Developmental Biology, Vanderbilt Medical Center, Nashville, Tennessee, USA; Veterans Affairs Medical Center, Nashville, Tennessee, USA; Department of Cancer Biology, Vanderbilt Medical Center, Nashville, Tennessee, USA. Electronic address: roy.zent@vanderbilt.edu.
3
Division of Nephrology, Department of Medicine, Vanderbilt Medical Center, Nashville, Tennessee, USA; Veterans Affairs Medical Center, Nashville, Tennessee, USA; Department of Cancer Biology, Vanderbilt Medical Center, Nashville, Tennessee, USA; Department of Molecular Physiology and Biophysics, Vanderbilt Medical Center, Nashville, Tennessee, USA.

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

PMID:
27773427
PMCID:
PMC5313325
DOI:
10.1016/j.kint.2016.08.025
[Indexed for MEDLINE]
Free PMC Article

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