巨噬细胞极化
癌症研究
巨噬细胞
肾
M2巨噬细胞
纤维化
IRF4公司
内科学
医学
免疫学
生物
髓样
转录因子
生物化学
基因
体外
作者
Kensuke Sasaki,Andrew S. Terker,Yu Pan,Zhilian Li,Shirong Cao,Yinqiu Wang,Aolei Niu,Suwan Wang,Xiaofeng Fan,Ming‐Zhi Zhang,Raymond C. Harris
出处
期刊:Journal of The American Society of Nephrology
日期:2021-02-22
卷期号:32 (5): 1037-1052
被引量:70
标识
DOI:10.1681/asn.2020071010
摘要
Deletion of Irf4 from myeloid cells protected against development of tubulointerstitial fibrosis after severe ischemic renal injury in mice, due primarily to inhibition of AKT-mediated monocyte recruitment to the injured kidney and reduced activation and subsequent polarization into a profibrotic M2 phenotype.
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