[Frontiers in Bioscience S2, 229-238, January 1, 2010]

EMT and TGF-beta in renal fibrosis

Masayuki Iwano

First Department of Internal Medicine, Nara Medical University, 840 Shijo, Kashihara, Nara 634-8522, Japan

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. Dissolution of cell-cell adhesion
4. Modulation of cell-ECM adhesion
5. EMT and TGF-1 signaling
6. EMT in the glomerulus
7. New therapeutic strategies aimed at inhibiting TGF-1-induced EMT
8. Conclusions
9. Acknowledgments
10. References

1. ABSTRACT

Transforming growth factor-beta1 (TGF-beta1) is a member of TGF-beta superfamily and the principal mediator contributing to the development and progression of renal fibrosis in a variety of disease settings. A critical effect of TGF-beta1 is the induction of epithelial-mesenchymal transition (EMT), which likely explains the continuous replenishment of fibroblasts during the progression of tissue fibrosis. Since we first identified EMT as the origin of fibroblasts in renal fibrosis, the signaling underlying EMT has been intensively studied in the field of nephrology. During the past five years, detailed mechanisms by which TGF-beta1 induces EMT have been clarified, and novel therapeutic approaches targeting TGF-beta1-mediated EMT are now being proposed.