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Uncovering the pathway of sepsis-induced renal tubular dysfunction. Focus on "Basolateral LPS inhibits NHE3 and HCOFormula absorption through TLR4/MyD88-dependent ERK activation in medullary thick ascending limb".

作者信息

Di Sole Francesca, Girardi Adriana C C

出版信息

Am J Physiol Cell Physiol. 2011 Dec;301(6):C1290-2. doi: 10.1152/ajpcell.00350.2011. Epub 2011 Sep 21.

DOI:10.1152/ajpcell.00350.2011
PMID:21940669
Abstract
摘要

相似文献

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Uncovering the pathway of sepsis-induced renal tubular dysfunction. Focus on "Basolateral LPS inhibits NHE3 and HCOFormula absorption through TLR4/MyD88-dependent ERK activation in medullary thick ascending limb".揭示脓毒症诱导的肾小管功能障碍的途径。聚焦于“髓袢升支粗段基底外侧脂多糖通过TLR4/MyD88依赖的ERK激活抑制NHE3和HCO₃⁻重吸收” 。
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2
Basolateral LPS inhibits NHE3 and HCOFormula absorption through TLR4/MyD88-dependent ERK activation in medullary thick ascending limb.基底外侧 LPS 通过 TLR4/MyD88 依赖的 ERK 激活抑制髓质升支粗段的 NHE3 和 HCOFormula 吸收。
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Lumen LPS inhibits HCO3(-) absorption in the medullary thick ascending limb through TLR4-PI3K-Akt-mTOR-dependent inhibition of basolateral Na+/H+ exchange.腔侧脂多糖通过 TLR4-PI3K-Akt-mTOR 依赖性抑制基底外侧 Na+/H+交换抑制髓质升支粗段的 HCO3(-) 吸收。
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High-mobility group box 1 inhibits HCO3- absorption in the medullary thick ascending limb through RAGE-Rho-ROCK-mediated inhibition of basolateral Na+/H+ exchange.高迁移率族蛋白盒1通过RAGE-Rho-ROCK介导的基底外侧Na+/H+交换抑制作用,抑制髓袢升支粗段的HCO3-重吸收。
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Aldosterone inhibits apical NHE3 and HCO3- absorption via a nongenomic ERK-dependent pathway in medullary thick ascending limb.醛固酮通过一种非基因组的、依赖细胞外信号调节激酶(ERK)的途径抑制髓袢升支粗段顶端的钠氢交换体3(NHE3)和碳酸氢根离子(HCO3-)的重吸收。
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A two-hit mechanism for sepsis-induced impairment of renal tubule function.脓毒症引起肾小管功能障碍的双打击机制。
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Hyposmolality stimulates Na(+)/H(+) exchange and HCO(3)(-) absorption in thick ascending limb via PI 3-kinase.低渗通过磷脂酰肌醇3激酶刺激髓袢升支粗段的钠/氢交换和碳酸氢根吸收。
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Nongenomic regulation by aldosterone of the epithelial NHE3 Na(+)/H(+) exchanger.醛固酮对上皮性钠氢交换蛋白3(NHE3)的非基因组调控
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Monophosphoryl lipid A induces protection against LPS in medullary thick ascending limb through a TLR4-TRIF-PI3K signaling pathway.单磷酰脂质A通过TLR4-TRIF-PI3K信号通路诱导髓质厚壁升支对脂多糖产生保护作用。
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引用本文的文献

1
Physiological aspects of Toll-like receptor 4 activation in sepsis-induced acute kidney injury.脓毒症诱导的急性肾损伤中Toll样受体4激活的生理学方面
Acta Physiol (Oxf). 2017 Mar;219(3):573-588. doi: 10.1111/apha.12798. Epub 2016 Oct 8.
2
Basolateral LPS inhibits NHE3 and HCOFormula absorption through TLR4/MyD88-dependent ERK activation in medullary thick ascending limb.基底外侧 LPS 通过 TLR4/MyD88 依赖的 ERK 激活抑制髓质升支粗段的 NHE3 和 HCOFormula 吸收。
Am J Physiol Cell Physiol. 2011 Dec;301(6):C1296-306. doi: 10.1152/ajpcell.00237.2011. Epub 2011 Aug 31.