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他米巴罗汀通过白介素-17A 抑制成纤维细胞的积累，从而减轻肾纤维化。

Tamibarotene inhibit the accumulation of fibrocyte and alleviate renal fibrosis by IL-17A.

机构信息

Department of Nephrology, Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Ren Fail. 2020 Nov;42(1):1173-1183. doi: 10.1080/0886022X.2020.1847145.

DOI:10.1080/0886022X.2020.1847145
PMID:33213229
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7737677/
Abstract

Renal fibrosis is a common pathological process in the progression of chronic kidney disease. Accumulating evidence suggests that interleukin-17A (IL-17A) and fibrocytes play crucial roles in the pathogenesis of fibrosis. However, the role of IL-17A in the regulation of renal fibrocytes in renal fibrosis has rarely been reported. Here, we report that the plasma IL-17A level is increased in immunoglobulin A nephropathy (IgAN) patients and is correlated with clinical parameters. Using a mouse model of unilateral ureteral obstruction (UUO), we found that both IL-17A expression and fibrocyte infiltration were increased in the kidneys of UUO mice. Besides, IL-17A enhanced fibrosis and fibrocyte-associated chemokine and activator expression . Furthermore, inhibition of IL-17A using Am80 (Tamibarotene) decreased fibrocytes and fibrocyte-associated chemokine and activator expression and significantly attenuated renal fibrosis in the UUO mice. Our findings suggest that Am80, which inhibits the accumulation of fibrocytes and alleviates renal fibrosis mediated by IL-17A, maybe a novel therapeutic drug for renal fibrosis.

摘要

肾纤维化是慢性肾脏病进展中的一种常见病理过程。越来越多的证据表明白细胞介素-17A（IL-17A）和纤维细胞在纤维化发病机制中起关键作用。然而，IL-17A 在调节肾纤维化中肾纤维细胞的作用很少有报道。在这里，我们报告说，免疫球蛋白 A 肾病（IgAN）患者的血浆 IL-17A 水平升高，并与临床参数相关。使用单侧输尿管梗阻（UUO）小鼠模型，我们发现 UUO 小鼠肾脏中 IL-17A 表达和纤维细胞浸润均增加。此外，IL-17A 增强了纤维化和纤维细胞相关趋化因子和激活剂的表达。此外，使用 Am80（Tamibarotene）抑制 IL-17A 可减少纤维细胞和纤维细胞相关趋化因子和激活剂的表达，并显著减轻 UUO 小鼠的肾纤维化。我们的研究结果表明，Am80 通过抑制纤维细胞的积累并减轻 IL-17A 介导的肾纤维化，可能成为治疗肾纤维化的一种新型治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/eee9f1214ebf/IRNF_A_1847145_F0006_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/71836cdae4fe/IRNF_A_1847145_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/868e833f954c/IRNF_A_1847145_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/d80744e5d249/IRNF_A_1847145_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/a7e862c096ce/IRNF_A_1847145_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/f35311fbc551/IRNF_A_1847145_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/eee9f1214ebf/IRNF_A_1847145_F0006_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/71836cdae4fe/IRNF_A_1847145_F0001_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/868e833f954c/IRNF_A_1847145_F0002_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/d80744e5d249/IRNF_A_1847145_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/a7e862c096ce/IRNF_A_1847145_F0004_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/f35311fbc551/IRNF_A_1847145_F0005_C.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/33cb/7737677/eee9f1214ebf/IRNF_A_1847145_F0006_C.jpg

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