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尿崩症中的水通道蛋白

Aquaporins in Diabetes Insipidus.

作者信息

Lu H A Jenny, He Jinzhao

机构信息

Program in Membrane Biology, Division of Nephrology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University-Peking University Joint Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, China.

出版信息

Adv Exp Med Biol. 2023;1398:267-279. doi: 10.1007/978-981-19-7415-1_18.

DOI:10.1007/978-981-19-7415-1_18
PMID:36717500
Abstract

Disruption of water and electrolyte balance is frequently encountered in clinical medicine. Regulating water metabolism is critically important. Diabetes insipidus (DI) presented with excessive water loss from the kidney is a major disorder of water metabolism. To understanding the molecular and cellular mechanisms and pathophysiology of DI and rationales of clinical management of DI is important for both research and clinical practice. This chapter will first review various forms of DI focusing on central diabetes insipidus (CDI) and nephrogenic diabetes insipidus (NDI). This is followed by a discussion of regulatory mechanisms underlying CDI and NDI, with a focus on the regulatory axis of vasopressin, vasopressin receptor 2 (V2R) and the water channel molecule, aquaporin 2 (AQP2). The clinical manifestation, diagnosis, and management of various forms of DI will also be discussed with highlights of some of the latest therapeutic strategies that are developed from in vitro experiments and animal studies.

摘要

水和电解质平衡紊乱在临床医学中屡见不鲜。调节水代谢至关重要。尿崩症(DI)表现为肾脏过度失水,是水代谢的一种主要紊乱疾病。了解尿崩症的分子和细胞机制、病理生理学以及临床管理的基本原理,对研究和临床实践都很重要。本章将首先回顾各种形式的尿崩症,重点是中枢性尿崩症(CDI)和肾性尿崩症(NDI)。随后将讨论CDI和NDI的调节机制,重点是抗利尿激素、抗利尿激素受体2(V2R)和水通道分子水通道蛋白2(AQP2)的调节轴。还将讨论各种形式尿崩症的临床表现、诊断和管理,并突出一些从体外实验和动物研究中开发的最新治疗策略。

相似文献

1
Aquaporins in Diabetes Insipidus.尿崩症中的水通道蛋白
Adv Exp Med Biol. 2023;1398:267-279. doi: 10.1007/978-981-19-7415-1_18.
2
Diabetes Insipidus.尿崩症
Adv Exp Med Biol. 2017;969:213-225. doi: 10.1007/978-94-024-1057-0_14.
3
New developments and concepts in the diagnosis and management of diabetes insipidus (AVP-deficiency and resistance).尿崩症(抗利尿激素缺乏和抵抗)诊断与管理的新进展和概念
J Neuroendocrinol. 2023 Jan;35(1):e13233. doi: 10.1111/jne.13233. Epub 2023 Jan 22.
4
[From genes to disease: from vasopressin-V2-receptor and aquaporine-2 to nephrogenic diabetes insipidus].[从基因到疾病:从血管加压素V2受体和水通道蛋白2到肾性尿崩症]
Ned Tijdschr Geneeskd. 2000 Dec 9;144(50):2402-4.
5
Vasopressin-independent targeting of aquaporin-2 by selective E-prostanoid receptor agonists alleviates nephrogenic diabetes insipidus.选择性 E 类前列腺素受体激动剂通过血管加压素非依赖性靶向水通道蛋白-2 来缓解肾性尿崩症。
Proc Natl Acad Sci U S A. 2011 Aug 2;108(31):12949-54. doi: 10.1073/pnas.1104691108. Epub 2011 Jul 18.
6
Genetic deletion of the nuclear factor of activated T cells 5 in collecting duct principal cells causes nephrogenic diabetes insipidus.集合管主细胞中激活 T 细胞核因子 5 的基因缺失导致肾性尿崩症。
FASEB J. 2022 Nov;36(11):e22583. doi: 10.1096/fj.202200856R.
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AKAPs-PKA disruptors increase AQP2 activity independently of vasopressin in a model of nephrogenic diabetes insipidus.AKAPs-PKA 抑制剂可在肾性尿崩症模型中独立于血管加压素增加 AQP2 的活性。
Nat Commun. 2018 Apr 12;9(1):1411. doi: 10.1038/s41467-018-03771-2.
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Activation of AQP2 water channels by protein kinase A: therapeutic strategies for congenital nephrogenic diabetes insipidus.蛋白激酶 A 对水通道蛋白 2 的激活:先天性肾性尿崩症的治疗策略。
Clin Exp Nephrol. 2021 Oct;25(10):1051-1056. doi: 10.1007/s10157-021-02108-6. Epub 2021 Jul 5.
9
Physiological insights into novel therapies for nephrogenic diabetes insipidus.对肾性尿崩症新疗法的生理学见解。
Am J Physiol Renal Physiol. 2016 Dec 1;311(6):F1149-F1152. doi: 10.1152/ajprenal.00418.2016. Epub 2016 Aug 17.
10
Nephrogenic Diabetes Insipidus.肾性尿崩症
Exp Suppl. 2019;111:317-339. doi: 10.1007/978-3-030-25905-1_15.

本文引用的文献

1
Diabetes Insipidus: Pathogenesis, Diagnosis, and Clinical Management.尿崩症:发病机制、诊断及临床管理
Cureus. 2021 Feb 23;13(2):e13523. doi: 10.7759/cureus.13523.
2
Acquired forms of central diabetes insipidus: Mechanisms of disease.获得性中枢性尿崩症:发病机制。
Best Pract Res Clin Endocrinol Metab. 2020 Sep;34(5):101449. doi: 10.1016/j.beem.2020.101449. Epub 2020 Jul 10.
3
Chlorpromazine Induces Basolateral Aquaporin-2 Accumulation via F-Actin Depolymerization and Blockade of Endocytosis in Renal Epithelial Cells.
氯丙嗪通过 F-肌动蛋白解聚和阻断内吞作用诱导肾上皮细胞基底外侧水通道蛋白-2 的积累。
Cells. 2020 Apr 23;9(4):1057. doi: 10.3390/cells9041057.
4
Gestational diabetes insipidus: Diagnosis and management.妊娠糖尿病性尿崩症:诊断与管理。
Best Pract Res Clin Endocrinol Metab. 2020 Sep;34(5):101384. doi: 10.1016/j.beem.2020.101384. Epub 2020 Feb 27.
5
Desmopressin and the risk of hyponatremia: A population-based cohort study.去氨加压素与低钠血症风险:基于人群的队列研究。
PLoS Med. 2019 Oct 21;16(10):e1002930. doi: 10.1371/journal.pmed.1002930. eCollection 2019 Oct.
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Diabetes insipidus.尿崩症。
Nat Rev Dis Primers. 2019 Aug 8;5(1):54. doi: 10.1038/s41572-019-0103-2.
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Arginine-stimulated copeptin measurements in the differential diagnosis of diabetes insipidus: a prospective diagnostic study.精氨酸刺激 copeptin 测量在尿崩症鉴别诊断中的作用:一项前瞻性诊断研究。
Lancet. 2019 Aug 17;394(10198):587-595. doi: 10.1016/S0140-6736(19)31255-3. Epub 2019 Jul 11.
8
ER-associated degradation is required for vasopressin prohormone processing and systemic water homeostasis.内质网相关降解对于血管加压素原激素加工和全身水平衡稳态是必需的。
J Clin Invest. 2017 Oct 2;127(10):3897-3912. doi: 10.1172/JCI94771. Epub 2017 Sep 18.
9
Vasopressin: physiology, assessment and osmosensation.血管加压素:生理学、评估和渗透压感知。
J Intern Med. 2017 Oct;282(4):284-297. doi: 10.1111/joim.12645. Epub 2017 Jul 26.
10
EGF Receptor Inhibition by Erlotinib Increases Aquaporin 2-Mediated Renal Water Reabsorption.厄洛替尼抑制表皮生长因子受体可增加水通道蛋白2介导的肾脏水重吸收。
J Am Soc Nephrol. 2016 Oct;27(10):3105-3116. doi: 10.1681/ASN.2015080903. Epub 2016 Mar 9.