食管黏膜下腺的双重作用：良性与恶性疾病中的保护与致病机制：一项范围综述
The Dual Roles of Esophageal Submucosal Glands: Protection and Pathogenesis in Benign and Malignant Disease: A Scoping Review.
文献信息
| PMID | 42882425 |
|---|---|
| 原文 | 在 PubMed 查看原文 ↗ |
| 发表日期 | 2026 |
| 作者 | Chun-Ting Chen |
| 作者单位 | Department of Gastroenterology and Hepatology, University Medical Centre Rotterdam (Erasmus MC), Erasmus University Rotterdam, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. |
| 期刊 | Cells |
| SCI 分区 | Q2 |
| IF | 6.6 |
| 研究类型 | 综述 Meta · 临床 |
| 所属专科 | 咽喉科 |
中文摘要
背景： 食管黏膜下腺（SMGs）通过分泌碳酸氢盐、黏蛋白和修复因子参与黏膜防御。慢性反流可能损害这些功能并重塑腺体区域，可能将SMG损伤与反流性食管炎、Barrett食管（BE）和食管腺癌（EAC）联系起来。
目的： 梳理关于食管SMGs生理和病理作用的人体、动物和体外文献，并识别与反流损伤、BE、EAC及内镜治疗相关的证据空白。
方法： 本范围综述按照PRISMA-ScR报告。检索Embase、Web of Science、PubMed和Google Scholar，从建库至2025年1月15日。两名评审员独立按照预设的纳入标准筛选记录。方案未注册。
结果： 本综述纳入97篇全文出版物和7篇会议摘要。全文集包括89项原始研究和8篇综述；综述文章用于背景和引文追溯，而非作为独立的一手证据计数。所梳理的文献支持SMGs的分泌和修复功能，并记录了损伤相关重塑，包括黏液性腺泡丢失和萎缩性、嗜酸细胞性或导管样表型的扩展。标志物表达、空间连续性和克隆观察与腺体参与修复和Barrett相关生物学相容，但并未确立独特的起源细胞，谱系关系仍未解决。
结论： 食管SMGs处于黏膜保护与病理可塑性之间的合理界面。最重要的空白是缺乏纵向人体证据、来源明确的谱系信息、腺体表型的标准化报告，以及能重现反流暴露和基质微环境的人体模型。
英文摘要
Background: Esophageal submucosal glands (SMGs) contribute to mucosal defense through bicarbonate, mucin, and reparative-factor secretion. Chronic reflux may impair these functions and remodel the glandular compartment, potentially linking SMG injury to reflux esophagitis, Barrett's esophagus (BE), and esophageal adenocarcinoma (EAC). Objective: To map the human, animal, and in vitro literature on the physiological and pathological roles of esophageal SMGs and to identify evidence gaps relevant to reflux injury, BE, EAC, and endoscopic therapy. Methods: This scoping review was reported in accordance with PRISMA-ScR. Embase, Web of Science, PubMed, and Google Scholar were searched from inception to 15 January 2025. Two reviewers independently screened records against prespecified eligibility criteria. The protocol was not registered. Results: The review included 97 full-text publications and 7 conference abstracts. The full-text set comprised 89 original studies and 8 reviews; review articles were used for context and citation tracing rather than counted as independent primary evidence. The mapped literature supports secretory and reparative functions of SMGs and documents injury-associated remodeling, including loss of mucinous acini and expansion of atrophic, oncocytic, or duct-like phenotypes. Marker expression, spatial continuity, and clonal observations are compatible with glandular participation in repair and Barrett-associated biology, but do not establish a unique cell of origin and lineage relationships remain unresolved. Conclusions: Esophageal SMGs occupy a plausible interface between mucosal protection and pathological plasticity. The most consequential gaps are the lack of longitudinal human evidence, source-resolved lineage information, standardized reporting of glandular phenotypes, and human models that reproduce reflux exposure and the stromal niche.