Fig. 2: Hepatic transcriptomic analysis and summary bioinformatics. | Nature Medicine

Fig. 2: Hepatic transcriptomic analysis and summary bioinformatics.

From: An integrated gene-to-outcome multimodal database for metabolic dysfunction-associated steatotic liver disease

Fig. 2

a, PCA plot for 616 MASLD samples and 34 normal liver control samples after including batch effects as covariates in the linear model. The first PC is displayed on the x axis and the second PC on the y axis, with the corresponding percentage of total variance explained by each PC. Dots represent individual samples colored according to NASH-CRN fibrosis stage. b, UpSet plot of DEGs showing the unique DEGs belonging to individual sets (fibrosis stages F0/1, F2, F3, F4) and the intersection of DEGs across all fibrosis stages. Set sizes are presented as bars, and their composition is described by the bottom panel. c,d, Dot plots showing the downregulated (c) and upregulated (d) Kyoto Encyclopedia of Genes and Genomes pathways (Benjamini and Hochberg false discovery rate q < 0.05 and fold-change of ≥1) obtained from one-sided gene-set-enrichment analysis for different fibrosis stages (F0/1, F2, F3, F4). The size of the dot is on the basis of gene count enriched in the pathway, and the color of the dot shows the pathway enrichment significance. e, FC of the top 20 differentially expressed genes in each fibrotic stage for both men and women. Exemplar dysregulated genes between men and women are highlighted for illustration. The gray color indicates that the genes were not statistically significantly dysregulated for that specific stage. f, Dot plot highlighting the differences between the Reactome pathways (q < 0.05 and FC ≥1) obtained by one-sided GSEA in men and women in stage F4 compared with controls. setSIZE indicates the total number of genes present in each specific gene set. P.adjust indicates the Benjamini and Hochberg adjusted P values. GeneRatio is k/n, where k is the overlap between the genes of interest and the gene set and n is the number of all unique genes of interest. CAM, cell adhesion molecule; ECM, extracellular matrix; HCM, hypertrophic cardiomyopathy; JAK, Janus kinase; MAPK, mitogen-activated protein kinase; STAT, signal transducer and activator of transcription.

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