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Wounding Smad

Nature Cell Biology volume 1, pages E117–E119 (1999)Cite this article

Abstract

TGF-β is a cytokine that enhances wound healing, a process involving diverse TGF-β-responsive cell types. Mice with a deletion of the Smad3 gene exhibit an increased rate of wound healing. The lack of Smad3 seems to modify the cellular response to TGF-β and may suggest an intriguing molecular basis to this process.

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Figure 1: The cellular basis for the accelerated re-epithelialization and faster wound healing in Smad3-deficient mice1.
Figure 2: The Smad2 and Smad3 arms of transforming growth factor-β (TGF-β) signalling in cells at a wound site, as inferred from the TGF-β-response phenotype of three cell types from Smad3-deficient animals1.

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Authors and Affiliations

  1. Cell Biology Program, Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, 10021, New York, USA

    Joan Massagué

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  1. Joan Massagué
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Massagué, J. Wounding Smad. Nat Cell Biol 1, E117–E119 (1999). https://doi.org/10.1038/12944

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