Fig. 4
From: Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis
The downregulation of DHX58 expression following I/R injury promotes ferroptosis in hepatocyte. a UMAP visualization of cells in the livers of Dhx58f/f and Dhx58hep−/− mice underwent sham or I/R, and each dot corresponded to one single cell colored according to the cell cluster. b The bubble diagram of signature genes for each cell type is displayed. UMAP visualization of hepatocytes in I/R-treated Dhx58f/f and Dhx58hep−/− mice was shown as indicated (c), cell counts of Dhx58f/f and Dhx58hep−/− mice in each hepatocyte cluster were shown (d), and functional gene enrichment in each hepatocyte cluster by QuSAGE analysis was shown (e). Liver I/R injury was administrated in Dhx58f/f and Dhx58hep/− mice, hepatic iron (f) and LPO (g) levels were analyzed accordingly (n = 4), representative transmission electron microscope images show the morphology of ferroptosis in hepatocyte with black arrows indicated mitochondrion and lipid droplets (h), GSH and GSSG were analyzed and the ratio was calculated (n = 4) (i). Scale bar = 20 μm (f) and 2 μm (h). j Serum ALT and AST of Dhx58f/f and Dhx58hep−/− mice treated with ferroptosis inducer erastin (n = 3). Data are shown as mean ± SD or photographs from one representative of three independent experiments. *P < 0.05, **P < 0.01. DHX58 DExH-box helicase 58, I/R ischemia/reperfusion, UMAP uniform manifold approximation and projection, QuSAGE quantitative set analysis of gene expression, LPO lipid peroxide, GSH glutathione, GSSG oxidized glutathione, ALT alanine aminotransferase, AST aspartate aminotransferase, SD standard deviation, HSEC hepatic sinusoid endothelium cell, GMP granulocyte-monocyte progenitor, NK natural killer, AIM2 absent in melanoma 2, NLRs nucleotide-binding leucine-rich repeat receptors, NLRP1 nucleotide-binding oligomerization domain-like receptor protein 1, IPAF interleukin-1β-converting enzyme-protease activating factor