APOLD1 and diabetic kidney disease: The upregulated DEGs in db/db mice were mainly clustered into lipid metabolism (such as Fat4, Elovl5, Apold1, Grem2, Stard13), IL-17A-dependent inflammation (Cxcl1, Tnf, Tnfsf9, Tnfrsf11a, Nfκbia, Nfkb2, Cpne5, Tspan6), fibrosis (Col4a5, Fgf12, Fgf15) and other DKD-related pathways indicating that changes at transcriptomics level captured the pathomechanism information about DKD.