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Nephrol Dial Transplant (2000) 15: 1729-1731
© 2000 European Renal Association-European Dialysis and Transplant Association


Editorial Comments

Transdifferentiation comes of age

Frank Strutz and Gerhard A. Müller

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 epithelial–mesenchymal 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. . . [Full Text of this Article]

In vivo evidence of tubular epithelial–mesenchymal transdifferentiation

Effects of matrix components and cytokines on transdifferentiation

Tubular epithelial transdifferentiation and proliferation

Acknowledgments

Notes

References


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