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UUO 诱导大鼠肺纤维化伴巨噬细胞-肌成纤维细胞转化。

UUO induces lung fibrosis with macrophage-myofibroblast transition in rats.

机构信息

Hebei University of Chinese Medicine, Shijiazhuang 050091, China; Hebei Key Laboratory of Integrative Medicine on Liver-Kidney Patterns, Institute of Integrative Medicine, College of Integrative Medicine, Hebei University of Chinese Medicine, Shijiazhuang 050091, China.

Hebei University of Chinese Medicine, Shijiazhuang 050091, China.

出版信息

Int Immunopharmacol. 2021 Apr;93:107396. doi: 10.1016/j.intimp.2021.107396. Epub 2021 Feb 1.

Abstract

Progression of chronic kidney disease (CKD) to uremia is often accompanied by varying degrees of lung damage and this is also an important cause of death. Although there are many studies on the mechanism of lung injury, it is not clearly understood. Inflammatory macrophages may associated with fibrosis in the lungs. Here, we investigated the role of macrophage-myofibroblast transition (MMT) in lung fibrosis with unilateral ureteral obstruction (UUO) rats. We found that cells undergoing MMT accounted for an important part of the myofibroblast population, and correlated with lung fibrosis, MMT cells in lungs have a predominant M2 phenotype, and this process was attenuated after treatment with eplerenone. In conclusion, our studies provide a possible mechanism for UUO-induced kidney damage and lung injury, indicating the possibility of using eplerenone, a mineralocorticoid receptor blocker, to treat UUO to reduce kidney damage and protect lung function.

摘要

慢性肾脏病(CKD)进展为尿毒症常伴有不同程度的肺损伤,这也是导致死亡的重要原因。虽然有很多关于肺损伤机制的研究,但并不清楚。炎症性巨噬细胞可能与肺纤维化有关。在这里,我们研究了巨噬细胞-肌成纤维细胞转化(MMT)在单侧输尿管梗阻(UUO)大鼠肺纤维化中的作用。我们发现,经历 MMT 的细胞占肌成纤维细胞群体的重要部分,与肺纤维化相关,肺中的 MMT 细胞具有占主导地位的 M2 表型,并且在用依普利酮治疗后,这一过程减弱。总之,我们的研究为 UUO 引起的肾损伤和肺损伤提供了一个可能的机制,表明使用盐皮质激素受体阻滞剂依普利酮治疗 UUO 以减少肾损伤和保护肺功能的可能性。

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