自噬
炎症
发病机制
肾病
免疫学
医学
抗体
生物
内分泌学
细胞凋亡
生物化学
糖尿病
作者
Mei‐Ying Chang,Xiujie Shi,Sijia Ma,Mingming Zhao,Fan Jiao,Zhiyu Pan,Shunxuan Xue,Ziyan Zhang,Zhenwei Shi,Bin Yang,Yu Zhang
标识
DOI:10.1016/j.ejphar.2023.176198
摘要
The pathogenesis of immunoglobulin A nephropathy (IgAN) is closely related to immunity and inflammation. The clinical process of IgAN varies greatly, making the assessment of prognosis challenging and limiting progress on effective treatment measures. Autophagy is an important pathway for the development of IgAN. However, the role of autophagy in IgAN is complex, and the consequences of autophagy may change during disease progression. In the present study, we evaluated the dynamic changes in autophagy during IgAN. Specifically, we examined autophagy in the kidney of a rat model of IgAN at different time points. We found that autophagy was markedly and persistently induced in IgAN rats, and the expression level of inflammation was also persistently elevated. The autophagy enhancer rapamycin and autophagy inhibitor 3-methyladenine were used in this study, and the results showed that 3-methyladenine can alleviate renal injury and inflammation in IgAN rats. Our study provides further evidence for autophagy as a therapeutic target for IgAN.
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