肠道的碳酸氢盐分泌和酸碱感应。

IF 2.9 4区 医学 Q2 PHYSIOLOGY Pflugers Archiv : European journal of physiology Pub Date : 2024-04-01 Epub Date: 2024-02-19 DOI:10.1007/s00424-024-02914-3
Holger M Becker, Ursula E Seidler
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引用次数: 0

摘要

碳酸氢盐在肠细胞膜上的转运调节着细胞内和管腔内的 pH 值,是肠道内液体定向运动的重要组成部分。自 20 世纪 70 年代首次描述 HCO3- 离子逆浓度梯度的 "主动 "转运以来,人们已认识到 HCO3- 转运对多种肠道功能的基本作用。离子转运蛋白已被确定并进行了分子鉴定,基因敲除小鼠模型也让人们深入了解了它们在多种功能中的各自作用。本综述介绍了过去十年中在肠道不同部分的肠道 HCO3- 转运分子调控的新技术和新发现方面取得的进展。我们讨论了存在肠道 HCO3- 分泌缺陷的人类疾病,以及提高管腔碱度的潜在治疗策略。综述的最后一部分强调了肠道酸碱感应的细胞和生物机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Bicarbonate secretion and acid/base sensing by the intestine.

The transport of bicarbonate across the enterocyte cell membrane regulates the intracellular as well as the luminal pH and is an essential part of directional fluid movement in the gut. Since the first description of "active" transport of HCO3- ions against a concentration gradient in the 1970s, the fundamental role of HCO3- transport for multiple intestinal functions has been recognized. The ion transport proteins have been identified and molecularly characterized, and knockout mouse models have given insight into their individual role in a variety of functions. This review describes the progress made in the last decade regarding novel techniques and new findings in the molecular regulation of intestinal HCO3- transport in the different segments of the gut. We discuss human diseases with defects in intestinal HCO3- secretion and potential treatment strategies to increase luminal alkalinity. In the last part of the review, the cellular and organismal mechanisms for acid/base sensing in the intestinal tract are highlighted.

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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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