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Mouse Kidney Transplantation: Models of Allograft Rejection
16:15

Mouse Kidney Transplantation: Models of Allograft Rejection

Published on: October 11, 2014

Epithelial-to-mesenchymal transition and chronic allograft tubulointerstitial fibrosis

Surmeet Bedi1, Aparna Vidyasagar, Arjang Djamali

  • 1Department of Medicine, Nephrology Section, University of Wisconsin Madison School of Medicine and Public Health, Madison, WI 53713, USA.

Transplantation Reviews (Orlando, Fla.)
|July 18, 2008
PubMed

Insights

Epithelial-to-mesenchymal transition (EMT) drives chronic kidney transplant fibrosis. Further research is needed to confirm EMT

Area of Science:

  • Nephrology
  • Transplantation Immunology
  • Cell Biology

Background:

  • Chronic allograft tubular atrophy/interstitial fibrosis (TA/IF) significantly contributes to late kidney allograft loss.
  • Identifying causes and developing targeted treatments for TA/IF are critical for advancing kidney transplantation.
  • Epithelial-to-mesenchymal transition (EMT) is increasingly recognized as a key process in kidney injury, including chronic allograft TA/IF.

Purpose of the Study:

  • To review the molecular and cellular pathways of EMT in the context of chronic allograft tubulointerstitial fibrosis.
  • To examine the roles of alloimmune T cells and oxidative stress in EMT-driven fibrosis.
  • To evaluate the potential of EMT as a marker for disease progression and discuss therapeutic strategies.

Main Methods:

  • Literature review focusing on molecular and cellular mechanisms of EMT in kidney allografts.
  • Analysis of studies investigating the influence of alloimmunity and oxidative stress on EMT.
  • Evaluation of existing data on EMT as a disease marker and therapeutic target.

Main Results:

  • EMT involves tubular epithelial cells transforming into myofibroblasts via loss of cell adhesion, altered gene expression (e.g., E-cadherin, alpha-smooth muscle actin), and extracellular matrix production.
  • Alloimmune T cells and oxidative stress are implicated in promoting EMT in kidney allografts.
  • EMT is demonstrably involved in the pathogenesis of chronic allograft tubulointerstitial fibrosis.

Conclusions:

  • EMT plays a significant role in the development of chronic allograft tubulointerstitial fibrosis.
  • The precise contribution of EMT to allograft fibrogenesis requires further investigation through interventional trials.
  • Additional research is necessary to validate EMT as a reliable surrogate marker for disease progression in kidney transplant recipients.

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