阴离子交换器 AE4(SLC4A9)的新功能。

IF 2.9 4区 医学 Q2 PHYSIOLOGY Pflugers Archiv : European journal of physiology Pub Date : 2024-04-01 Epub Date: 2024-01-09 DOI:10.1007/s00424-023-02899-5
Helga Vitzthum, Catherine Meyer-Schwesinger, Heimo Ehmke
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摘要

肾脏在酸碱平衡中起着至关重要的作用。在远端肾小球中,α间质细胞分泌尿酸(H+),β间质细胞分泌尿碱(HCO3-)。β间叶细胞通过调节顶端Cl-/HCO3-交换体pendrin(SLC26A4)的活性来调节酸碱状态。在这篇综述中,我们总结并讨论了我们目前对肾脏转运体 AE4(SLC4A9)生理作用的认识。AE4 作为阳离子依赖性 Cl-/HCO3- 交换子,只在β间质细胞的基底侧膜上表达,对小鼠代谢性酸碱紊乱的感知至关重要,但对肾脏钠重吸收和血浆容量控制却不重要。本文讨论了可能将通过 AE4 进行的基底侧酸碱感应与顶端垂体素活性联系起来的潜在细胞内信号传导途径。
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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Novel functions of the anion exchanger AE4 (SLC4A9).

The kidney plays a crucial role in acid-base homeostasis. In the distal nephron, α-intercalated cells contribute to urinary acid (H+) secretion and β-intercalated cells accomplish urinary base (HCO3-) secretion. β-intercalated cells regulate the acid base status through modulation of the apical Cl-/HCO3- exchanger pendrin (SLC26A4) activity. In this review, we summarize and discuss our current knowledge of the physiological role of the renal transporter AE4 (SLC4A9). The AE4, as cation-dependent Cl-/HCO3- exchanger, is exclusively expressed in the basolateral membrane of β-intercalated cells and is essential for the sensing of metabolic acid-base disturbances in mice, but not for renal sodium reabsorption and plasma volume control. Potential intracellular signaling pathways are discussed that might link basolateral acid-base sensing through the AE4 to apical pendrin activity.

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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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