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Contribution of Wound-Associated Cells and Mediators in Orchestrating Gastrointestinal Mucosal Wound Repair.
Annual Review of Physiology ( IF 15.7 ) Pub Date : 2018-10-24 , DOI: 10.1146/annurev-physiol-020518-114504
Miguel Quirós 1 , Asma Nusrat 1
Affiliation  

The gastrointestinal mucosa, structurally formed by the epithelium and lamina propria, serves as a selective barrier that separates luminal contents from the underlying tissues. Gastrointestinal mucosal wound repair is orchestrated by a series of spatial and temporal events that involve the epithelium, recruited immune cells, resident stromal cells, and the microbiota present in the wound bed. Upon injury, repair of the gastrointestinal barrier is mediated by collective migration, proliferation, and subsequent differentiation of epithelial cells. Epithelial repair is intimately regulated by a number of wound-associated cells that include immune cells and stromal cells in addition to mediators released by luminal microbiota. The highly regulated interaction of these cell types is perturbed in chronic inflammatory diseases that are associated with impaired wound healing. An improved understanding of prorepair mechanisms in the gastrointestinal mucosa will aid in the development of novel therapeutics that promote mucosal healing and reestablish the critical epithelial barrier function.

中文翻译:

伤口相关细胞和介质在协调胃肠粘膜伤口修复中的贡献。

胃肠粘膜在结构上由上皮和固有层形成,充当将管腔内容物与下面的组织分开的选择性屏障。胃肠粘膜伤口修复是由一系列空间和时间事件精心策划的,这些事件涉及上皮、招募的免疫细胞、驻留基质细胞和伤口床中存在的微生物群。损伤后,胃肠道屏障的修复是由上皮细胞的集体迁移、增殖和随后的分化介导的。上皮修复受到许多伤口相关细胞的密切调节,其中包括免疫细胞和基质细胞以及腔内微生物群释放的介质。这些细胞类型之间高度调控的相互作用在与伤口愈合受损相关的慢性炎症性疾病中受到干扰。加深对胃肠粘膜修复机制的了解将有助于开发促进粘膜愈合和重建关键上皮屏障功能的新型疗法。
更新日期:2019-02-11
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