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• W2155994292 abstract "Over the last 3 decades, the incidence of esophageal adenocarcinoma has dramatically increased in Western countries; a similar increase may be observed in Asian countries in the near future. Esophageal adenocarcinoma arises from a sequential gastroesophageal reflux disease (GERD) spectrum from reflux erosive esophagitis, to Barrett's esophagus, and finally to esophageal adenocarcinoma. At present, gastric acid and bile are assumed to be primarily involved in the etiology of the GERD spectrum. We reported in 2002 that, at the gastroesophageal junction in humans, abundant amounts of nitric oxide (NO) are generated luminally through the entero-salivary re-circulation of dietary nitrate. Since then, we have carried out a series of experiments to demonstrate that NO diffuses into the adjacent epithelium at cytotoxic levels. This diffusion results in disruption of the epithelial barrier function, exacerbation of inflammation, acceleration of columnar transformation in the esophagus (Barrett's esophagus) via the induction of caudal-type homeobox 2, and the shifting of carcinogenic N-nitroso compound formation from the luminal to epithelial compartment. These results suggest that, in addition to conventionally recognized causative factors, luminal NO could also be involved in the pathogenesis of the GERD spectrum. In addition, we recently showed that there is a prominent gender-related difference in NO-related cytotoxicity in the esophagus and that estrogen attenuated the esophageal tissue damage via the estrogen receptor in female rats. The role of estrogen in attenuating the esophageal tissue damage in NO-related esophageal damage could explain the well-recognized male predominance in the GERD spectrum in humans." @default.
• W2155994292 created "2016-06-24" @default.
• W2155994292 creator A5018653096 @default.
• W2155994292 creator A5029930183 @default.
• W2155994292 date "2014-04-21" @default.
• W2155994292 modified "2023-10-02" @default.
• W2155994292 title "Involvement of luminal nitric oxide in the pathogenesis of the gastroesophageal reflux disease spectrum" @default.
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• W2155994292 doi "https://doi.org/10.1111/jgh.12548" @default.
• W2155994292 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24863184" @default.
• W2155994292 hasPublicationYear "2014" @default.
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