Wingate Institute of Neurogastroenterology, Blizard Institute, Faculty of Medicine and Dentistry, Queen Mary University of London, London E1 4NS, UK.
Int J Mol Sci. 2023 Jan 28;24(3):2502. doi: 10.3390/ijms24032502.
Gastroesophageal reflux disease (GORD) affects up to 20% of Western populations, yet sensory mechanisms underlying heartburn pathogenesis remain incompletely understood. While central mechanisms of heartburn perception have been established in earlier studies, recent studies have highlighted an important role of neurochemical, inflammatory, and cellular changes occurring in the oesophageal mucosa itself. The localization and neurochemical characterisation of sensory afferent nerve endings differ among GORD phenotypes, and could explain symptom heterogeneity among patients who are exposed to similar levels of reflux. Acid-induced stimulation of nociceptors on pain-sensing nerve endings can regulate afferent signal transmission. This review considers the role of peripheral mechanisms of sensitization in the amplification of oesophageal sensitivity in patients with GORD.
胃食管反流病（GORD）影响了高达 20%的西方人群，但烧心发病机制的感觉机制仍不完全清楚。虽然早期研究已经确定了烧心感知的中枢机制，但最近的研究强调了食管黏膜本身发生的神经化学、炎症和细胞变化的重要作用。在 GORD 表型中，感觉传入神经末梢的定位和神经化学特征不同，这可以解释暴露于相似反流水平的患者之间症状的异质性。酸诱导对痛觉神经末梢上伤害感受器的刺激可以调节传入信号的传递。这篇综述考虑了外周致敏机制在 GORD 患者食管敏感性放大中的作用。
