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Epithelial-mesenchymal transition (EMT) in kidney fibrosis: fact or fantasy?
Wilhelm Kriz, Brigitte Kaissling, Michel Le Hir
Wilhelm Kriz, Brigitte Kaissling, Michel Le Hir
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Personal perspective

Epithelial-mesenchymal transition (EMT) in kidney fibrosis: fact or fantasy?

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Abstract

Epithelial-mesenchymal transition (EMT) has become widely accepted as a mechanism by which injured renal tubular cells transform into mesenchymal cells that contribute to the development of fibrosis in chronic renal failure. However, an increasing number of studies raise doubts about the existence of this process in vivo. Herein, we review and summarize both sides of this debate, but it is our view that unequivocal evidence supporting EMT as an in vivo process in kidney fibrosis is lacking.

Authors

Wilhelm Kriz, Brigitte Kaissling, Michel Le Hir

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Figure 1

In the kidney, FSP1/S100A4 does not stain fibroblasts or myofibroblast.

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In the kidney, FSP1/S100A4 does not stain fibroblasts or myofibroblast.
...
(A) Double immunofluorescence for S100A4 (red channel) and ecto-5′nucleotidase (5′NT, green channel) and (B) for S100A4 (red channel) and α-SMA (green channel); nuclei in B are stained by DAPI. (A) 3-mm-thick cryostat section of renal cortex (rat); the thick arrow points to a 5′NT-positive interstitial fibroblast; S100A4-positive cells (thin arrows) are seen inside capillaries. Scale bar: ~10 mm. Reproduced with permission from Histochemistry and Cell Biology (15). (B) Renal cortex after 4 days of ureteral obstruction (rat); no cellular colocalization of S100A4 and α-SMA. G, glomerulus. Inset: S100A4-positive cells, showing strong cytoplasmic and weak nuclear staining; the shape of the cells is reminiscent of migrating lymphocytes. Scale bars: ~100 mm; inset, ~10 mm. Reproduced with permission from Histochemistry and Cell Biology (17).

Copyright © 2026 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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