Deletion of Myeloid Interferon Regulatory Factor 4 (Irf4) in Mouse Model Protects against Kidney Fibrosis after Ischemic Injury by Decreased Macrophage Recruitment and Activation.
Kensuke SasakiAndrew S TerkerYu PanZhilian LiShirong CaoYinqiu WangAolei NiuSuwan WangXiaofeng FanMing-Zhi ZhangRaymond C HarrisPublished in: Journal of the American Society of Nephrology : JASN (2021)
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.
Keyphrases
- dendritic cells
- mouse model
- induced apoptosis
- immune response
- signaling pathway
- ischemia reperfusion injury
- bone marrow
- cell cycle arrest
- cell proliferation
- adipose tissue
- transcription factor
- acute myeloid leukemia
- liver fibrosis
- cerebral ischemia
- metabolic syndrome
- endoplasmic reticulum stress
- type diabetes
- peripheral blood
- pi k akt