Despite gastro‐esophageal reflux disease affecting up to 20% of Western populations, relatively little is known about the molecular mechanisms underlying its most troublesome symptom: heartburn. Recent findings have unveiled the role of components of the esophageal mucosa in the pathogenesis of GERD including sensory nociceptive nerves and inflammatory mediators. Erosive esophagitis was long believed to develop as a result of acid injury at the esophageal lumen, but novel concepts suggest the generation of reflux‐induced esophageal injury as a result of cytokine‐mediated inflammation. Moreover, the localization and characterization of mucosal afferent nerves vary between GERD phenotypes and could explain the heterogeneity of symptom perception between patients who experience similar levels of acid reflux.

中文翻译：

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胃食管反流病的黏膜发病机制

尽管胃食管反流病影响了多达 20% 的西方人群，但对其最棘手症状的分子机制知之甚少：胃灼热。最近的研究结果揭示了食管黏膜成分在 GERD 发病机制中的作用，包括感觉伤害神经和炎症介质。长期以来，人们认为糜烂性食管炎是食管腔酸损伤的结果，但新概念表明细胞因子介导的炎症会导致反流引起的食管损伤。此外，粘膜传入神经的定位和特征因 GERD 表型而异，可以解释经历相似酸反流水平的患者之间症状感知的异质性。