Experimental and Molecular Medicine (Apr 2018)

IL-33/ST2 axis mediates hyperplasia of intrarenal urothelium in obstructive renal injury

  • Wei-Yu Chen,
  • Jenq-Lin Yang,
  • Yi-Hsiu Wu,
  • Lung-Chih Li,
  • Ru-Fang Li,
  • Ya-Ting Chang,
  • Lo-Hsin Dai,
  • Wan-Chen Wang,
  • Ya-Jen Chang

DOI
https://doi.org/10.1038/s12276-018-0047-8
Journal volume & issue
Vol. 50, no. 4
pp. 1 – 11

Abstract

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Urology: Tracking a trigger for kidney damage An inflammatory signaling protein may play an important role in kidney damage associated with urinary tract blockage. Untreated obstructive nephropathy can lead to kidney injury, particularly in younger patients. Taiwanese researchers led by Wei-Yu Chen at the Kaohsiung Chang Gung Memorial Hospital and Ya-Jen Chang at the Academia Sinica, Taipei, homed in on a signaling pathway that apparently contributes to the pathology of this condition. Using an animal model of surgically induced obstructive nephropathy, the researchers observed a post-injury spike in production of an immunity-activating protein called interleukin (IL)-33. This protein subsequently activates a host of immune cell types, and also stimulates abnormal growth in a subset of urinary tract epithelial cells. This excessive growth may directly contribute to subsequent damage and functional impairment of the kidney, although more research will be needed to confirm this.