Key Results:
Hyperuricemia-related CKD was characterized by the rise in serum uric
acid, decline in renal function, macrophage alternative (M2)
polarization, and kidney fibrosis. Integrated bioinformatic analyses
revealed ITGAM as the potential core gene mediating disease progression
which was associated with FAK/Akt1/β-catenin signaling. Notably, we
confirmed the upregulated macrophage ITGAM, activated pathway, and
macrophage M2 polarization in injured kidneys and Raw 264.7 macrophages.
In vitro, we verified ITGAM/FAK/Akt1/β-catenin pathway participated in
promoting macrophage M2 polarization through silencing Itgam and
inhibiting FAK or Akt1 phosphorylation, where the expression of M2
phenotype macrophage markers and downstream molecules in pathway were
down-regulated.