Fig. 2. Il11 knockout mice are protected from epithelial–mesenchymal transition and renal pathology following acute kidney injury.

a Schematic of acute kidney injury (AKI) induction by FA administration in Il11^−/− and WT mice for experiments shown in (b–i). A single dose of FA (200 mg/kg) or an equivalent volume of vehicle control (0.3 M NaHCO₃) was administered intraperitoneally, and the mice were sacrificed at D28. b Western blots showing renal expression of IL11, IL11RA1, pERK, ERK, pSTAT3, STAT3, pp90RSK, p90RSK, pGSK3β, GSK3β, SNAI1, ZEB, E-Cadherin, Cyclin D1, αSMA, Fibronectin (FN1), and GAPDH (representative dataset from n = 5/group), c representative kidney gross anatomy, d representative Masson’s Trichrome images of whole kidney cross section (scale bars: 500 µm, representative dataset from n = 3/group), e kidney weights, f kidney collagen content by hydroxyproline assay, g blood urea nitrogen (BUN) levels, h urine albumin-to-creatinine ratios (ACRs), and i relative renal mRNA expression of kidney injury markers (Ngal, Kim1) and pro-inflammatory markers (Tnfα, Il6, Ccl2, Ccl5, Il1β). e–i Data are shown as box-and-whisker with median (middle line), 25th–75th percentiles (box), and minimum–maximum values (whiskers); WT-NaHCO₃, Il11^−/− -NaHCO₃ (n = 5/group), WT-FA (n = 6), Il11^−/− -FA (n = 7); two-way ANOVA with Sidak’s correction. FC: Fold change. Source data are provided as a Source data file.