English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Gastroesophageal reflux (GER) disease is a chronic disease characterized by the recurrent ascension of some of the gastric contents in the esophagus. Indeed, gastric acid secreted by parietal cells and the gastric pepsin activity, but not the intestinal alkaline content, are the most important pathogenic factors of GER. Several pathophysiological mechanisms are involved, the most important of which is the imbalance of the redox state of the esophageal tissue. Indeed, several studies have shown that reflux esophagitis is mediated by oxygen-derived free radicals. In this chapter, we describe the pathophysiology and important pathways, especially acid gastric contents and reactive oxygen species involved in pathology of GER.

The Role of Increased Gastric Acid Secretion and Reactive Oxygen Species in the Pathophysiology of Reflux Esophagitis