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The gastroesophageal junction is the region where the esophagus meets the stomach, formed by the anatomical and physiological structures of the lower esophageal sphincter (LES) and the crural diaphragm. Its main function is to act as a barrier to prevent the backflow (reflux) of gastric acid and stomach contents into the esophagus. Disruption of this barrier zone, impairment of LES function, or increased gastric acid production can result in diseases such as gastroesophageal reflux disease (GERD), esophagitis, and, in chronic cases, Barrett’s esophagus or esophageal cancer[1][2][4]. While this region is important for maintaining normal digestive tract physiology and is associated with several disease processes, it is not itself a molecular or receptor-based therapeutic target, and “gastric acid and gastroesophageal junction” is not an accepted canonical name for a drug target.
Acid secretion inhibitors (proton pump inhibitors, H2 receptor antagonists) reduce acidity; antacids neutralize acid. Drugs may increase tone (prokinetics), or reduce transient sphincter relaxations.
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