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中华肥胖与代谢病电子杂志 ›› 2025, Vol. 11 ›› Issue (04) : 337 -343. doi: 10.3877/cma.j.issn.2095-9605.2025.04.012

综述

肥胖合并胃食管反流病的分子机制研究进展
温家鑫1, 艾克拜尔·艾力1,2,3,4,()   
  1. 1830054 乌鲁木齐,新疆医科大学研究生学院
    2830002 乌鲁木齐,新疆维吾尔自治区人民医院微创、疝和腹壁外科
    3830002 乌鲁木齐,新疆胃食管反流病与减重代谢外科临床医学研究中心
    4830002 乌鲁木齐,新疆维吾尔自治区普外微创研究所
  • 收稿日期:2025-03-25 出版日期:2025-11-30
  • 通信作者: 艾克拜尔·艾力
  • 基金资助:
    新疆维吾尔自治区重点研发任务专项-厅厅联动项目(2023B03010-3); "天山英才"医药卫生高层次人才培养计划(TSYC202301A011)

Research progress on molecular mechanism of obesity complicated with gastroesophageal reflux disease

Jiaxin Wen1, Aili Aikebaier·1,2,3,4,()   

  1. 1Graduate School of Xinjiang Medical University, Urumqi 830054, China
    2Department of Minimally Invasive Surgery, Hernia and Abdominal Surgery, People's Hospital of Xinjiang Uygur Autonomous Region, 830002 Urumqi, China
    3Xinjiang Gastroesophageal Reflux Disease and Weight Loss Metabolic Surgery Clinical Medical Research Center, 830002 Urumqi, China
    4Institute of Minimally Invasive Surgery, Xinjiang Uygur Autonomous Region, 830002 Urumqi, China
  • Received:2025-03-25 Published:2025-11-30
  • Corresponding author: Aili Aikebaier·
引用本文:

温家鑫, 艾克拜尔·艾力. 肥胖合并胃食管反流病的分子机制研究进展[J/OL]. 中华肥胖与代谢病电子杂志, 2025, 11(04): 337-343.

Jiaxin Wen, Aili Aikebaier·. Research progress on molecular mechanism of obesity complicated with gastroesophageal reflux disease[J/OL]. Chinese Journal of Obesity and Metabolic Diseases(Electronic Edition), 2025, 11(04): 337-343.

肥胖是胃食管反流病(GERD)和食管裂孔疝的独立危险因素。尽管已从解剖及生理学层面阐明了两者关联,但其深层的分子机制仍待深入探索。本文旨在系统综述当前关于肥胖驱动GERD的分子机制研究进展,重点探讨炎症微环境、代谢重编程、肠道菌群失调及相关信号通路的交互作用,以期为理解其病理生理学提供整合性视角,并为临床防治策略提供新思路。

Obesity is an established independent risk factor for gastroesophageal reflux disease (GERD) and hiatal hernia. Although the relationship between obesity and these conditions has been clarified from anatomical and physiological perspectives, the underlying molecular mechanisms require further elucidation. This review aims to systematically summarize current research progress on the molecular mechanisms driving obesity-induced GERD, with a focus on the interplay among inflammatory microenvironments, metabolic reprogramming, intestinal flora dysbiosis, and related signaling pathways. This integrated perspective seeks to enhance understanding of the pathophysiology and thereby inform novel clinical prevention and treatment strategies.

图1 脂肪细胞诱导食管炎症机制注:浸润在脂肪细胞的单核巨噬细胞和被瘦素、CD4+T细胞活化的ASC皆可过表达IL-6、TNF-α等炎症因子,这些炎症因子能激活MAPK和JAK-STAT信号通路加重食管黏膜炎症反应。
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