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. 2023 Dec 5;134(4):e172963. doi: 10.1172/JCI172963

Figure 6. Genetic deletion or pharmacological inhibition of FASN or ACSS2 attenuates inflammasome activation.

Figure 6

(A) Transcript levels of Nlrp3, IL1B, IL18, and Gsdmd in control and UUO kidneys of Fasnfl/fl Ksp Cre (n = 6) and WT (n = 4) mice. (B) Immunoblots of NLRP3, CASP1, P20 (cleaved caspase 1), GSDMD-F, GSDMD-N, and GAPDH expression in UUO kidneys from WT and Fasnfl/fl Ksp Cre mice. (C) Experimental design. (D) Transcript levels of Nlrp3, IL1B, IL18, and Gsdmd in UUO kidneys of mice injected with ACSS2i (n = 3) or vehicle (n = 3). (E) Immunoblots showing NLRP3, CASP1, P20, GSDMD-F, GSDMD-N, and GAPDH expression in UUO kidneys from mice injected with vehicle (n = 3) or ACSS2i (n = 3). (F) Experimental design. (G) Transcript levels of Nlrp3, IL1B, IL18, and Gsdmd in WT (n = 6) and Acss2–/– (n = 7) mice following UUO surgery. (H) Immunoblots showing NLRP3, CASP1, P20, GSDMD-F, GSDMD-N, and GAPDH expression in UUO kidneys from WT and Acss2–/– mice. (I) Transcript levels of Nlrp3, IL1B, IL18, and Gsdmd in adenine-treated CKD kidneys from WT (n = 7) and Acss2–/– (n = 6) mice. (J) Immunoblots showing NLRP3, CASP1, P20, GSDMD-F, GSDMD-N, and GAPDH expression in adenine-treated CKD kidneys from WT and Acss2–/– mice. Data are presented as the mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001, by 1-way ANOVA after Tukey’s multiple-comparison test (A, D, G, and I). Data in A were log2 transformed. The protein marker was cropped from all blots but is presented in the full blots file.