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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Hepatic ischemia/reperfusion injury disrupts the homeostasis of kidney primary cilia via oxidative stress
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Hepatic ischemia/reperfusion injury disrupts the homeostasis of kidney primary cilia via oxidative stress

机译:肝缺血/再灌注损伤通过氧化应激扰乱肾脏原发性纤毛的稳态

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摘要

Acute kidney injury (AKI) is a major complication of hepatic surgeries. The primary cilium protrudes to the lumen of kidney tubules and plays an important role in renal functions. Disruption of primary cilia homeostasis is highly associated with human diseases including AKI. Here, we investigated whether transient hepatic ischemia induces length change and deciliation of kidney primary cilia, and if so, whether reactive oxygen species (ROS)/oxidative stress regulates those. HIR induced damages to the liver and kidney with increases in ROS/oxidative stress. HIR shortened the cilia of kidney epithelial cells and caused them to shed into the urine. This shortening and shedding of cilia was prevented by Mn(III) tetrakis(1-methyl-4-pyridyl) porphyrin (MnTMPyP, an antioxidant). The urine of patient undergone liver resection contained ciliary proteins. These findings indicate that HIR induces shortening and deciliation of kidney primary cilia into the urine via ROS/oxidative stress, suggesting that primary cilia is associated with HIR-induced AKI and that the presence of ciliary proteins in the urine could be a potential indication of kidney injury.
机译:急性肾损伤(AKI)是肝脏手术的主要复杂性。原发性纤维突出到肾小管小管的内腔,并在肾功能中起重要作用。原发性纤毛宿主的破坏与包括AKI在内的人类疾病高度相关。在这里,我们研究了疾病肝缺血是否诱导肾脏原发性纤毛的长度变化和脱落,如果是这样,是否可以进行反应性氧(ROS)/氧化应激调节那些。 HIR诱导对肝肾和肾脏的损害,随着ROS /氧化应激的增加。 HIR缩短了肾上皮细胞的纤毛,并使它们落入尿液中。通过Mn(III)四(1-甲基-4-吡啶基)卟啉(MNTmpyp,抗氧化剂)防止这种脆弱和脱落。患者的尿液经过肝切除含有睫状蛋白。这些发现表明,HIR通过ROS /氧化应激诱导肾脏原发性纤毛的肾脏原发性纤毛释放到尿液中,表明原发性纤毛与HIR诱导的AKI有关,并且尿液中睫状蛋白的存在可能是肾脏的潜在指示受伤。

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