Gastroduodenal injury and repair: novel targets for therapeutic intervention.
Gastroduodenal injury and repair: novel targets for therapeutic intervention.
复制标题
胃十二指肠损伤与修复：治疗干预的新靶点。
DOI：
10.1097/mog.0000000000000883
复制
发表时间：
2022-11-01
影响因子：
2.5
通讯作者：
Hagen, Susan J.
中科院分区：
文献类型：
--
作者：
Hagen, Susan J.
尽管粘膜屏障是环境和宿主之间的主要界面，但对于急性、浅表病变或更深、持续性病变的修复知之甚少，如果不愈合，这些病变可能是腔内抗原、炎症和/或肿瘤发展的通透性增加的部位。最近的研究集中在黏附激酶上，它在浅表损伤恢复过程中调控基质黏附。肌动蛋白聚合调节细胞迁移，肌动蛋白相关蛋白的重要性也被强调。对SARS-CoV-2感染的研究为covid-19感染患者的胃十二指肠黏膜损伤提供了重要的新见解，对类器官和芯片肠道的研究为冠状病毒如何感染胃肠道组织及其导致的屏障功能障碍提供了新的认识。提出了一种新的风险分层模式，以协助胃溃疡或十二指肠溃疡患者进行重复内镜检查的决策，并研究了溃疡疾病的新治疗方案。最后，利用新型转基因小鼠模型对深度损伤和壁细胞丢失后皮化生的发生机制进行了研究。最近的研究强调了促进胃十二指肠黏膜损伤后粘膜愈合的新分子靶点。
Although the mucosal barrier serves as a primary interface between the environment and host, little is understood about the repair of acute, superficial lesions or deeper, persistent lesions that if not healed, can be the site of increased permeability to luminal antigens, inflammation, and/or neoplasia development. Recent studies have focused on focal adhesion kinase, which regulates controlled matrix adhesion during restitution after superficial injury. Actin polymerization regulates cell migration and the importance of actin-related proteins was also highlighted. Work on SARS-CoV-2 infection lent important new insights on gastroduodenal mucosal injury in patients with covid-19 infection and work done with organoids and intestine-on-a-chip contributed new understanding about how coronaviruses infect GI tissues and its resulting barrier dysfunction. A novel risk stratification paradigm was proposed to assist with decision making about repeat endoscopy for patients with gastric or duodenal ulcers and new therapeutic options were studied for ulcer disease. Lastly, work to support the mechanism of metaplasia development after deep injury and parietal cell loss was provided using novel transgenic mouse models. Recent studies highlight novel molecular targets to promote mucosal healing after injury of the gastroduodenal mucosa.