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首页> 外文期刊>Advances in clinical chemistry >Fetal skin wound healing.
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Fetal skin wound healing.

机译：胎儿皮肤伤口愈合。

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The developing fetus has the ability to heal wounds by regenerating normal epidermis and dermis with restoration of the extracellular matrix (ECM) architecture, strength, and function. In contrast, adult wounds heal with fibrosis and scar. Scar tissue remains weaker than normal skin with an altered ECM composition. Despite extensive investigation, the mechanism of fetal wound healing remains largely unknown. We do know that early in gestation, fetal skin is developing at a rapid pace and the ECM is a loose network facilitating cellular migration. Wounding in this unique environment triggers a complex cascade of tightly controlled events culminating in a scarless wound phenotype of fine reticular collagen and abundant hyaluronic acid. Comparison between postnatal and fetal wound healing has revealed differences in inflammatory response, cellular mediators, cytokines, growth factors, and ECM modulators. Investigation into cell signaling pathways and transcription factors has demonstrated differences in secondary messenger phosphorylation patterns and homeobox gene expression. Further research may reveal novel genes essential to scarless repair that can be manipulated in the adult wound and thus ameliorate scar.
机译：发育中的胎儿具有通过恢复正常的表皮和真皮恢复细胞外基质（ECM）结构，强度和功能来治愈伤口的能力。相反，成人伤口会随着纤维化和疤痕愈合。随着ECM成分的改变，疤痕组织仍比正常皮肤弱。尽管进行了广泛的研究，但胎儿伤口愈合的机制仍然未知。我们确实知道，在妊娠早期，胎儿皮肤正在快速发展，而ECM是促进细胞迁移的疏松网络。在这种独特的环境中受伤会触发一系列严格控制的事件，最终形成细网状胶原蛋白和丰富的透明质酸的无创伤口表型。产后和胎儿伤口愈合的比较显示出炎症反应，细胞介质，细胞因子，生长因子和ECM调节剂的差异。对细胞信号通路和转录因子的研究表明，次级信使磷酸化模式和同源盒基因表达存在差异。进一步的研究可能揭示无痕修复必不可少的新基因，该基因可以在成人伤口中进行操作，从而减轻疤痕。

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