Fig. 9
From: Knockdown of hepatic mitochondrial calcium uniporter mitigates MASH and fibrosis in mice

RNA-sequencing analysis and protein immunoblotting indicate the molecular mechanisms involving in targeting MCU for treatment MASH and fibrosis. A GO enrichment analysis of the differentially expressed genes (DEGs) in livers between MCU knockdown MASH mice and wild-type (WT) MASH mice. n = 3 mice. B KEGG pathway and oncogenes enrichment analysis for the DEGs; and top 9 KEGG pathway from enrichment analysis are shown. The false discovery rate (FDR)-adjusted P-value was indicated. C Western blots for p-MOB1, MOB1, p-LATS1/2, LATS1/2, p-AMPK/AMPK, p-YAP, and YAP in the whole liver from indicated mice; and β-actin serves as a loading control. D Densitometric analyses of blots for p-LATS/LATS, p-MOB1/MOB1, p-AMPK/AMPK, and p-YAP/YAP in livers. All data are presented as the mean ± SD. P-value are for two-way ANOVA with Tukey’s test. *P < 0.05, **P < 0.01, and ***P < 0.001; ns indicates not significant