Fig. 2: Positive associations between hepatic Ly6d expression and steatosis in both mice and humans.
From: LY6D is crucial for lipid accumulation and inflammation in nonalcoholic fatty liver disease
A Immunofluorescence images showing increased Ly6d expression in the livers of both HSD- and HFD-fed mice. Scale bar: 50 μm. B Volcano plots depicting the correlation (Spearman’s rho, x-axis) between hepatic Ly6d expression and all available phenotypes in the BXD mouse genetic reference population, as well as statistical significance levels (–log10[p value], y-axis). C Pathological findings in human liver tissues from the GTEx liver data, ranging from no steatosis to severe steatosis, with disease severity weighted in terms of LY6d expression levels. D Representative images of H&E staining of human liver tissues from the GTEx liver data. E Heatmaps of gene expression levels of liver DEGs related to NAFLD and NASH between subjects with high Ly6d expression and those with low Ly6d expression. The false discovery rate (FDR) was determined by the Benjamini‒Hochberg (BH) procedure. F Bar chart summarizing the pathway enrichment analysis of DEGs. HSD high-sucrose high-fat diet, HFD high-fat diet, H&E hematoxylin and eosin, NAFLD nonalcoholic fatty liver disease, NASH nonalcoholic steatohepatitis, DEGs differentially expressed genes.
