Elucidation of the healing mechanism for developing gene therapy in palatal wounds

腭裂患者在婴儿期手术修复后，常会出现上颌骨生长发育障碍和牙弓狭窄。这被认为是在腭部伤口愈合过程中形成的疤痕的结果。Smad3是转化生长因子-b信号通路的成员之一，Smad3基因缺陷的小鼠表现出明显的促进腭部损伤创面愈合的作用，本研究探讨了Smad3磷酸化的特异性抑制剂在创伤修复中的作用，结果发现创面愈合加速，炎症基因下调。

Cleft palate patients are often subject to maxillary growth impairment and narrow dental arch after surgical closure of the defect in infancy. This is considered to be a consequence of the scar which is formed during palatal wound healing. Smad3 is one of the members concerned to TGF-b signaling pathway, and its deficient mice showed the notably accelerated wound healing in injured palates.In this study, we investigated the effects of a specific inhibitor of Smad3 phosphorylation in wound repair, and as a result, an accelerated wound closure with down regulation of inflammatory genes was observed.