#6562 ITGAM PROMOTES MACROPHAGE ALTERNATIVE ACTIVATION IN HYPERURICEMIA-RELATED CHRONIC KIDNEY DISEASE
نویسندگان
چکیده
Abstract Background and Aims Hyperuricemia is an essential risk factor in chronic kidney disease (CKD), while urate-lowering therapy to prevent or delay CKD progression controversial. Alternatively activated macrophages response local microenvironment play diverse roles injury, repair, fibrosis. Here, we aim investigate whether how macrophage ITGAM contributes hyperuricemia-related CKD. Method In vivo, explored dynamic characteristics of renal tissue By incorporating mRNA protein sequencing data, analyzed gene expression profile, hub genes potential pathways responsible for development, which was further confirmed using qPCR, western blotting, immunofluorescent stainings. vitro, validated bioinformatic findings under different conditions with interventions corresponding core nodes pathway. Results Hyperuricemia-related characterized by the rise serum uric acid, decline function, alternative (M2) polarization, Integrated analyses revealed as mediating associated FAK/Akt1/β-catenin signaling. Notably, upregulated ITGAM, pathway, M2 polarization injured kidneys Raw 264.7 macrophages. verified ITGAM/FAK/Akt1/β-catenin pathway participated promoting through silencing Itgam inhibiting FAK Akt1 phosphorylation, where phenotype markers downstream molecules were down-regulated. Conclusion CKD, promotes contributing fibrosis signaling Targeting might be a promising therapeutic approach preventing delaying
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ژورنال
عنوان ژورنال: Nephrology Dialysis Transplantation
سال: 2023
ISSN: ['1460-2385', '0931-0509']
DOI: https://doi.org/10.1093/ndt/gfad063c_6562