Transepithelial Fluid and Salt Re-Absorption Regulated by cGK2 Signals.

Transepithelial Fluid and Salt Re-Absorption Regulated by cGK2 Signals.
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cGK2 信号调节跨上皮液体和盐的重吸收

DOI:
10.3390/ijms19030881
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发表时间:
2018-03-16
影响因子:
5.6
通讯作者:
Ji HL
Ji HL
中科院分区:
生物学2区
文献类型:
--
作者:
Chang J;Ding Y;Zhou Z;Nie HG;Ji HL

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上皮组织中的跨上皮液体和盐重吸收在液体和盐稳态中起重要作用。在吸收上皮中,液体和盐通量由主要由上皮钠通道(ENaC)、囊性纤维化跨膜传导调节因子(CFTR)、Na+/H+交换器(NHE)、水通道蛋白和钠钾腺苷三磷酸酶(Na+/K+-ATP酶)组成的机制控制。跨上皮的液体和盐转运的失调有助于许多疾病的发病机制,例如肺水肿和囊性纤维化。细胞内和细胞外信号,即,激素和蛋白激酶,调节液体和盐的周转和解决。越来越多的证据表明,跨上皮液体转运受环磷酸鸟苷依赖性蛋白激酶(cGK)信号的调节。cGK 2最初是从肠道标本中鉴定和克隆的,其存在也已在肾脏和肺中得到证实。cGK 2通过ENaC、CFTR和NHE调节液体和盐。在急性肺损伤中观察到cGK 2对跨上皮离子转运的调节不足,并且cGK 2可能是恢复上皮组织中水肿障碍的新的药物靶点。
Transepithelial fluid and salt re-absorption in epithelial tissues play an important role in fluid and salt homeostasis. In absorptive epithelium, fluid and salt flux is controlled by machinery mainly composed of epithelial sodium channels (ENaC), cystic fibrosis transmembrane conductance regulator (CFTR), Na+/H+ exchanger (NHE), aquaporin, and sodium potassium adenosine triphosphatase (Na+/K+-ATPase). Dysregulation of fluid and salt transport across epithelium contributes to the pathogenesis of many diseases, such as pulmonary edema and cystic fibrosis. Intracellular and extracellular signals, i.e., hormones and protein kinases, regulate fluid and salt turnover and resolution. Increasing evidence demonstrates that transepithelial fluid transport is regulated by cyclic guanosine monophosphate-dependent protein kinase (cGK) signals. cGK2 was originally identified and cloned from intestinal specimens, the presence of which has also been confirmed in the kidney and the lung. cGK2 regulates fluid and salt through ENaC, CFTR and NHE. Deficient cGK2 regulation of transepithelial ion transport was seen in acute lung injury, and cGK2 could be a novel druggable target to restore edematous disorder in epithelial tissues.
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