Health Science Center, Ningbo University, Ningbo, 315211, People's Republic of China.
Ningbo No.2 Hospital, Ningbo, 315001, People's Republic of China.
J Transl Med. 2024 Jan 31;22(1):123. doi: 10.1186/s12967-024-04932-2.
Esophageal strictures significantly impair patient quality of life and present a therapeutic challenge, particularly due to the high recurrence post-ESD/EMR. Current treatments manage symptoms rather than addressing the disease's etiology. This review concentrates on the mechanisms of esophageal stricture formation and recurrence, seeking to highlight areas for potential therapeutic intervention.
A literature search was conducted through PUBMED using search terms: esophageal stricture, mucosal resection, submucosal dissection. Relevant articles were identified through manual review with reference lists reviewed for additional articles.
Preclinical studies and data from animal studies suggest that the mechanisms that may lead to esophageal stricture include overdifferentiation of fibroblasts, inflammatory response that is not healed in time, impaired epithelial barrier function, and multimethod factors leading to it. Dysfunction of the epithelial barrier may be the initiating mechanism for esophageal stricture. Achieving perfect in-epithelialization by tissue-engineered fabrication of cell patches has been shown to be effective in the treatment and prevention of esophageal strictures.
The development of esophageal stricture involves three stages: structural damage to the esophageal epithelial barrier (EEB), chronic inflammation, and severe fibrosis, in which dysfunction or damage to the EEB is the initiating mechanism leading to esophageal stricture. Re-epithelialization is essential for the treatment and prevention of esophageal stricture. This information will help clinicians or scientists to develop effective techniques to treat esophageal stricture in the future.
食管狭窄显著降低患者的生活质量，并带来治疗上的挑战，尤其是内镜下黏膜切除术（ESD）/内镜黏膜下剥离术（EMR）后较高的复发率。目前的治疗方法主要针对症状，而非针对疾病的病因。本综述集中探讨食管狭窄形成和复发的机制，以期突出潜在治疗干预的靶点。
通过 PUBMED 以“食管狭窄、黏膜切除术、黏膜下剥离术”等术语进行文献检索，通过手动审查相关文章，并查阅参考文献以获取其他文章。
临床前研究和动物研究数据表明，导致食管狭窄的机制可能包括成纤维细胞过度分化、未能及时愈合的炎症反应、上皮屏障功能受损以及多因素导致的狭窄。上皮屏障功能障碍可能是食管狭窄的起始机制。通过组织工程制造细胞贴片来实现完美的上皮内化已被证明可有效治疗和预防食管狭窄。
食管狭窄的发展涉及三个阶段：食管上皮屏障（EEB）的结构损伤、慢性炎症和严重纤维化，其中 EEB 的功能障碍或损伤是导致食管狭窄的起始机制。再上皮化对于食管狭窄的治疗和预防至关重要。这些信息将有助于临床医生或科学家在未来开发有效的治疗食管狭窄的技术。
