Insight into molecular mechanisms underlying hepatic dysfunction in severe COVID-19 patients using systems biology

Figure 3 functional clustering analysis of the upregulated transcriptome of severe coronavirus disease 2019 patients liver autopsy tissues. A: Heatmap representation of the differentially upregulated genes and subsequently enriched pathways and functional clusters in severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infected liver samples in comparison to baseline expression in healthy tissue samples; B and C: Heatmap representation of the log2 of normalized expression of transcripts implicated signaling through (B) Class A-rhodopsin-like receptors and (C) Class F-frizzled and smoothened receptors; D: Box plot representation of some of the top upregulated transcripts in SARS-CoV-2 infected liver tissue samples. Data presented as mean ± SE; ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, ^dP < 0.0005, ^eP < 0.0001 coronavirus disease 2019 (COVID-19) vs Healthy. DNAJB1: DnaJ heat shock protein family (hsp40) member b1; IGF2: Insulin growth factor 2; SCARNA10: Small cajal body-specific rna 10; HSP90AB1: Heat shock protein 90 alpha family class B member 1; HDGF: Hepatoma-derived growth factor; SDHA: Succinate dehydrogenase complex flavoprotein subunit A.