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首页> 外文期刊>International Journal of Molecular Sciences >Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury
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Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury

机译:Vasohibin-2的遗传缺失加剧了缺血再灌注诱导的急性肾损伤

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Acute kidney injury (AKI) has been increasingly recognized as a risk factor for transition to chronic kidney disease. Recent evidence suggests that endothelial damage in peritubular capillaries can accelerate the progression of renal injury. Vasohibin-2 (VASH2) is a novel proangiogenic factor that promotes tumor angiogenesis. However, the pathophysiological roles of VASH2 in kidney diseases remain unknown. In the present study, we examined the effects of VASH2 deficiency on the progression of ischemia–reperfusion (I/R) injury-induced AKI. I/R injury was induced by bilaterally clamping renal pedicles for 25 min in male wild-type (WT) and Vash2 homozygous knockout mice. Twenty-four hours later, I/R injury-induced renal dysfunction and tubular damage were more severe in VASH2-deficient mice than in WT mice, with more prominent neutrophil infiltration and peritubular capillary loss. After induction of I/R injury, VASH2 expression was markedly increased in injured renal tubules. These results suggest that VASH2 expression in renal tubular epithelial cells might be essential for alleviating I/R injury-induced AKI, probably through protecting peritubular capillaries and preventing inflammatory infiltration.
机译:急性肾脏损伤(AKI)越来越被认为是过渡到慢性肾病的危险因素。最近的证据表明,腹膜毛细血管内皮损伤可以加速肾损伤的进展。 vasohibin-2(Vash2)是一种新的促进肿瘤血管生成的促进因子。然而,Vash2在肾病中的病理生理作用仍然未知。在本研究中,我们检查了Vash2缺乏对缺血再灌注进展(I / R)损伤诱发的AKI的影响。在雄性野生型(WT)和VASH2纯合敲除小鼠中,双侧夹住肾胞胎诱导I / R损伤。二十四小时后,Vash2缺陷小鼠的I / R损伤诱导肾功能紊乱和管状损伤比在WT小鼠中更严重,中性粒细胞渗透和梗死毛细血管损失更显着。在诱导I / R损伤后,受损肾小管中的VASH2表达明显增加。这些结果表明,肾小管上皮细胞的Vash2表达可能对于缓解I / R损伤诱导的AKI可能是必不可少的,可能是通过保护梗死毛细血管和预防炎症浸润。

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