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. 2016 Nov 21;127(1):321–334. doi: 10.1172/JCI87532

Figure 6. IRAK4 inhibition attenuates inflammatory and fibrotic responses in vivo and improves organ function.

Figure 6

(A–C) Effect of kidney IRI and BIIB-IRAK4i (inh) on whole-kidney transcriptional responses at 7 days after injury showing inflammatory genes (A), epithelial injury marker (B), and Col1a1 (C). (D–I) Representative histological and immunofluorescence images (D–F) and quantitative analysis of kidneys from IRI at day 7 after injury treated with BIIB-IRAK4i compared with vehicle or sham control kidneys. (G–I) Quantification of tubular injury, interstitial fibrosis, and extent of myofibroblasts detected by αSMA. (J) Quantification of kidney weight changes associated with unilateral IRI. Ratios of ischemic kidneys’ to contralateral (CL) kidneys’ weights 14 days after injury are shown. (K) Measurement of glomerular filtration rate (GFR) by creatinine clearance (CrCl) in post-IRI kidney at 16 days, following contralateral nephrectomy at 14 days. (Scale bars: 50 μm; n = 3–11 per group; *P < 0.05, 2-tailed Student’s t test or 2-way ANOVA, Bonferroni’s multiple comparisons test.)