镁在肾脏中的重吸收。

IF 3.7 2区 医学 Q1 PHYSIOLOGY American Journal of Physiology-renal Physiology Pub Date : 2023-03-01 DOI:10.1152/ajprenal.00298.2022
Jeroen H F de Baaij
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引用次数: 2

摘要

Mg2+对许多细胞和生理过程至关重要,包括肌肉收缩、神经元活动和代谢。因此,血液中Mg2+浓度受到肠道Mg2+吸收、肾脏Mg2+排泄以及骨骼和软组织中Mg2+储存平衡的严格调节。近年来,新型转基因动物模型的开发和孟德尔疾病的鉴定,使我们对肾脏中Mg2+重吸收的分子机制有了更深入的了解。在近端小管中,Mg2+的重吸收依赖于claudin-2/12的细胞旁通透性。在Henle’s环的厚升肢中,claudin-16/19复合体为细胞旁的Mg2+再吸收提供了一个阳离子选择性孔。细胞旁的Mg2+重吸收在这段是由Ca2+感应受体,甲状旁腺激素和雷帕霉素(mTOR)信号的机制靶点调节。在远曲小管中,Mg2+重吸收的微调是通过瞬时受体电位美拉抑素样6型和7型(TRPM6/TRPM7)二价阳离子通道进行的。TRPM6/TRPM7的活性依赖于激素调节、代谢活性和相互作用蛋白。基底侧Mg2+挤压仍然知之甚少,但可能依赖于Na+梯度。Cyclin M2和SLC41A3是Na+/Mg2+交换剂的主要候选分子。因此,基底外侧Na+/K+运输的紊乱间接导致远曲小管肾Mg2+重吸收受损。总之,本文综述了Mg2+在肾脏中再吸收的分子机制,特别关注转基因小鼠模型和人类遗传性疾病。
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Magnesium reabsorption in the kidney.

Mg2+ is essential for many cellular and physiological processes, including muscle contraction, neuronal activity, and metabolism. Consequently, the blood Mg2+ concentration is tightly regulated by balanced intestinal Mg2+ absorption, renal Mg2+ excretion, and Mg2+ storage in bone and soft tissues. In recent years, the development of novel transgenic animal models and identification of Mendelian disorders has advanced our current insight in the molecular mechanisms of Mg2+ reabsorption in the kidney. In the proximal tubule, Mg2+ reabsorption is dependent on paracellular permeability by claudin-2/12. In the thick ascending limb of Henle's loop, the claudin-16/19 complex provides a cation-selective pore for paracellular Mg2+ reabsorption. The paracellular Mg2+ reabsorption in this segment is regulated by the Ca2+-sensing receptor, parathyroid hormone, and mechanistic target of rapamycin (mTOR) signaling. In the distal convoluted tubule, the fine tuning of Mg2+ reabsorption takes place by transcellular Mg2+ reabsorption via transient receptor potential melastatin-like types 6 and 7 (TRPM6/TRPM7) divalent cation channels. Activity of TRPM6/TRPM7 is dependent on hormonal regulation, metabolic activity, and interacting proteins. Basolateral Mg2+ extrusion is still poorly understood but is probably dependent on the Na+ gradient. Cyclin M2 and SLC41A3 are the main candidates to act as Na+/Mg2+ exchangers. Consequently, disturbances of basolateral Na+/K+ transport indirectly result in impaired renal Mg2+ reabsorption in the distal convoluted tubule. Altogether, this review aims to provide an overview of the molecular mechanisms of Mg2+ reabsorption in the kidney, specifically focusing on transgenic mouse models and human hereditary diseases.

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来源期刊
CiteScore
8.40
自引率
7.10%
发文量
154
审稿时长
2-4 weeks
期刊介绍: The American Journal of Physiology - Renal Physiology publishes original manuscripts on timely topics in both basic science and clinical research. Published articles address a broad range of subjects relating to the kidney and urinary tract, and may involve human or animal models, individual cell types, and isolated membrane systems. Also covered are the pathophysiological basis of renal disease processes, regulation of body fluids, and clinical research that provides mechanistic insights. Studies of renal function may be conducted using a wide range of approaches, such as biochemistry, immunology, genetics, mathematical modeling, molecular biology, as well as physiological and clinical methodologies.
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