Gastric mucosal injuries include focal and diffused injuries, which do and do not change the cell differentiation pattern. Parietal cells loss is related to the occurrence of gastric mucosal diffused injury, with two phenotypes of spasmolytic polypeptide-expressing metaplasia and neuroendocrine cell hyperplasia, which is the basis of gastric cancer and gastric neuroendocrine tumor respectively. Multiple ion channels and transporters are located and expressed in the parietal cells, which is not only regulate the gastric acid-base homeostasis, but also regulate the growth and development of parietal cells. Therefore, alteration and dysregulation of ion channels and transporters in the parietal cells impairs the morphology and physiological functions of stomach, resulted in gastric diffused mucosal damage. In this review, multiple ion channels and transporters in parietal cells, including K ⁺ channels, aquaporins, Cl ^- channels, Na ⁺ /H ⁺ transporters, and Cl ^- /HCO ₃ ^- transporters are described, and their roles in gastric diffused mucosal injury are discussed. We hope to drive researcher’s attention to focus on the role of ion channels/transporters loss in the parietal cells induced gastric diffused mucosal injury.

Dysfunction of ion channels and transporters in the parietal cells induced two phenotypes of gastric diffused mucosal injury. (Red arrows indicate downregulation and black arrows indicate upregulation; SPEM: spasmolytic polypeptide-expressing metaplasia; IM: intestinal metaplasia; G-NET: gastric neuroendocrine tumor.)