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To determine the role of Smad3 in mediating the fibrotic response induced by TGF-beta.

Smad3 as a mediator of the fibrotic response

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To determine the role of Smad3 in mediating the fibrotic response induced by TGF-beta.
Used mice with targeted deletion of Smad3 to evaluate fibrotic responses.
Examined responses to TGF-beta-induced EMT and fibrosis in several animal models.
Tested small molecule inhibitors and overexpression of inhibitory Smad7 for therapeutic potential.
Smad3 null mice were resistant to various fibrosis models including radiation and bleomycin.
TGF-beta-mediated EMT and gene expression for collagens were significantly impaired in Smad3 null mice.
Inhibition of Smad3 reduced fibrotic responses in kidney, lung, and liver models.

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Randomized trial shows that Smad3 is crucial for mediating fibrosis across several models, indicating potential treatment targets.

Kathleen C. Flanders (2004) studied this question.

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