盐皮质激素受体
肌成纤维细胞
依普利酮
医学
纤维化
肺
病理
肾脏疾病
肺纤维化
肾
人口
巨噬细胞
内科学
受体
生物
环境卫生
体外
生物化学
作者
Fan Yang,Yi Chang,Cuijuan Zhang,Yunzhao Xiong,Xiangting Wang,Xuelian Ma,Zheng Wang,Hui Li,Tatsuo Shimosawa,Lin Pei,Qingyou Xu
标识
DOI:10.1016/j.intimp.2021.107396
摘要
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.
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