髓袢升支粗段
Thick ascending limb of the loop of Henle.
作者信息
Mount David B
机构信息
Renal Division, Brigham and Women's Hospital, Veterans Affairs Boston Healthcare System, Boston, Massachusetts
出版信息
Clin J Am Soc Nephrol. 2014 Nov 7;9(11):1974-86. doi: 10.2215/CJN.04480413. Epub 2014 Oct 15.
Abstract
The thick ascending limb occupies a central anatomic and functional position in human renal physiology, with critical roles in the defense of the extracellular fluid volume, the urinary concentrating mechanism, calcium and magnesium homeostasis, bicarbonate and ammonium homeostasis, and urinary protein composition. The last decade has witnessed tremendous progress in the understanding of the molecular physiology and pathophysiology of this nephron segment. These advances are the subject of this review, with emphasis on particularly recent developments.
摘要
髓袢升支粗段在人体肾脏生理学中占据核心的解剖学和功能位置，在细胞外液量的维持、尿液浓缩机制、钙和镁的稳态、碳酸氢盐和铵的稳态以及尿蛋白组成方面发挥着关键作用。在过去十年中，人们对这个肾单位节段的分子生理学和病理生理学的理解取得了巨大进展。这些进展是本综述的主题，重点是特别近期的发展。
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本文引用的文献
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Common variants in UMOD associate with urinary uromodulin levels: a meta-analysis.UMOD基因的常见变异与尿调节蛋白水平相关：一项荟萃分析。
J Am Soc Nephrol. 2014 Aug;25(8):1869-82. doi: 10.1681/ASN.2013070781. Epub 2014 Feb 27.
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Common noncoding UMOD gene variants induce salt-sensitive hypertension and kidney damage by increasing uromodulin expression.常见的非编码 UMOD 基因变异通过增加尿调蛋白的表达引起盐敏感性高血压和肾脏损伤。
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Angiotensin II stimulates basolateral 10-pS Cl channels in the thick ascending limb.血管紧张素 II 刺激升支粗段基底外侧 10-pS Cl 通道。
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Uromodulin upregulates TRPV5 by impairing caveolin-mediated endocytosis.尿调素通过损害窖蛋白介导的内吞作用而上调 TRPV5。
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Activation of the Ca(2+)-sensing receptor increases renal claudin-14 expression and urinary Ca(2+) excretion.钙敏感受体的激活增加了肾脏紧密连接蛋白-14 的表达和尿钙排泄。
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Calcium-binding protein 39 facilitates molecular interaction between Ste20p proline alanine-rich kinase and oxidative stress response 1 monomers.钙结合蛋白 39 促进 Ste20p 脯氨酸丙氨酸丰富激酶和氧化应激反应 1 单体之间的分子相互作用。
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Deficiency of the calcium-sensing receptor in the kidney causes parathyroid hormone-independent hypocalciuria.肾脏钙敏感受体缺失导致甲状旁腺激素不依赖性低钙尿。
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