Abstract

The cytosolic calcium ([Ca2+]cyt) is one of the most important cell signaling that can modulate gastrointestinal (GI) epithelial secretion and promote GI mucosal wound repair. The GI mucosal bicarbonate secretion is the main mechanism of mucosal protection. Our research team has been working in this field and provided solid evidence for the important role of Ca2+ signaling in the regulation of GI epithelial secretion and the underlying molecular mechanisms. In this review, we attempt to systemically review the current status of our knowledge on the role of Ca2+ signaling in the regulation of intestinal bicarbonate secretion and in the upper GI epithelial protection. We expect that novel targets could be identified for drug development to better protect GI mucosa and treat mucosal injury with the advance in this filed.

Highlights

  • Cytosolic free Ca2+ ([Ca2+]cyt) plays an essential role in a variety of mammalian cells through the regulation of many biological functions, including neurotransmitter release, muscle contraction, gene regulation, cell proliferation, and apoptosis [1]

  • Ca2+ release from intracellular stores is mediated by ryanodine receptor (RyR) and inositol triphosphate receptor (IP3R) channels

  • Acid-sensitive ion channel functions represent duodenal epithelial cells and can be stimulated by acid-stimulated HCO3– through the Ca2+ signaling pathway [55]. (iv) CFTR: CFTR expression is essential for HCO3– secretion by most of the gastrointestinal epithelial tissue; in these epithelial cells, a large proportion of the transport of transgene material, including HCO3, is mediated through the electrical diffusion pathway, suggesting that anion channels are involved in this process

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Summary

Introduction

Cytosolic free Ca2+ ([Ca2+]cyt) plays an essential role in a variety of mammalian cells through the regulation of many biological functions, including neurotransmitter release, muscle contraction, gene regulation, cell proliferation, and apoptosis [1]. The cytosolic calcium ([Ca2+]cyt) is one of the most important cell signaling that can modulate gastrointestinal (GI) epithelial secretion and promote GI mucosal wound repair. We attempt to systemically review the current status of our knowledge on the role of Ca2+ signaling in the regulation of intestinal bicarbonate secretion and in the upper GI epithelial protection.

Results
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