| First Author | Ashcroft GS | Year | 2000 |
| Journal | Cytokine Growth Factor Rev | Volume | 11 |
| Issue | 1-2 | Pages | 125-31 |
| PubMed ID | 10708960 | Mgi Jnum | J:61301 |
| Mgi Id | MGI:1354661 | Doi | 10.1016/s1359-6101(99)00036-2 |
| Citation | Ashcroft GS, et al. (2000) Loss of Smad3 modulates wound healing. Cytokine Growth Factor Rev 11(1-2):125-31 |
| abstractText | TGF-beta plays a central and critical role in tissue repair. The recent identification of TGF-beta signal transduction pathways involving Smad proteins has now made it possible to explore their contribution to the activities of TGF-beta in vivo. Both Smad3 and its closely related homolog Smad2 act as latent nuclear transcriptional activators and mediate intracellular signaling by TGF-betas and activin, each of which regulates cellular functions pivotal to cutaneous wound healing. Mice null for Smad3 (Smad3(ex8/ex8)) survive into adulthood and show accelerated cutaneous wound healing characterized by an increased rate of re-epithelialization and a reduced local inflammatory infiltrate. These data implicate Smad3 in specific pathways of tissue repair and suggest that it could be a target for the development of therapeutic strategies to modulate wound healing. |
