Nephrol Dial Transplant (2000) 15: 1729-1731
© 2000 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Transdifferentiation comes of age
Department of Nephrology and Rheumatology, Georg-August-University Medical Center, Robert-Koch-Str. 40, D-37075 Göttingen, Germany
Introduction
Five years ago we wrote an editorial in this journal about the possible transdifferentiation of tubular epithelial cells to fibroblasts [1]. We had just cloned a fibroblast specific protein (FSP)-1 in murine kidney fibroblasts and had described that de novo expression of this protein could be detected in selected tubular epithelial cells during late stages of renal fibrogenesis, indicating possible epithelialmesenchymal transformation (EMT) or transdifferentiation [2]. After this passage of time, we would like to readdress the issue of transdifferentiation and the scientific evidence collected in the meantime supporting its existence.
As was pointed out in that first editorial, transdifferentiation is defined as the loss of one phenotype and the acquisition of a new one. Transdifferentiation is a physiological process during development but has also been described in a number of adult organs including the liver, the thyroid and the mammary glands (reviewed in [3
In vivo evidence of tubular epithelialmesenchymal transdifferentiation
Effects of matrix components and cytokines on transdifferentiation
Tubular epithelial transdifferentiation and proliferation
Acknowledgments
Notes
References
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