Roles of interferon regulatory factor 4 in the AKI-CKD transition, glomerular diseases and kidney allograft rejection

被引:4
|
作者
Song, Jianling [1 ]
Ke, Ben [1 ]
Tu, Weiping [1 ]
Fang, Xiangdong [1 ,2 ]
机构
[1] Nanchang Univ, Dept Nephrol, Affiliated Hosp 2, Nanchang, Jiangxi, Peoples R China
[2] Nanchang Univ, Dept Nephrol, Affiliated Hosp 2, 1,Minde Rd, Nanchang, Jiangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
Interferon regulatory factor 4; AKI-CKD transition; glomerular disease; kidney allograft rejection; TRANSCRIPTION FACTOR IRF4; PLASMA-CELL DIFFERENTIATION; LONG-TERM SURVIVAL; IGA NEPHROPATHY; LUPUS NEPHRITIS; GENE-EXPRESSION; INJURY; ASSOCIATION; RECEPTOR; MECHANISMS;
D O I
10.1080/0886022X.2023.2259228
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Interferon regulatory factor 4 (IRF4) is expressed in immune cells and is a member of the interferon regulatory factor family. Recently, it has been found that IRF4 plays important roles in the acute kidney injury (AKI)-chronic kidney disease (CKD) transition, glomerular diseases and kidney allograft rejection. In particular, the relationship between IRF4 and the AKI-CKD transition has attracted widespread attention. Furthermore, it was also found that the deficiency of IRF4 hindered the transition from AKI to CKD through the suppression of macrophage-to-fibroblast conversion, inhibition of M1-M2 macrophage polarization, and reduction in neutrophil inward flow. Additionally, an examination of the crucial role of IRF4 in glomerular disease was conducted. It was reported that inhibiting IRF4 could alleviate the progression of glomerular disease, and potential physiopathology mechanisms associated with IRF4 were postulated. Lastly, IRF4 was found to have detrimental effects on the development of antibody-mediated rejection (ABMR) and T-cell-mediated rejection (TCMR).
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页数:10
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