Fig. 6: Ire1α deficiency reduces ischemic kidney damage.
From: IRE1α determines ferroptosis sensitivity through regulation of glutathione synthesis
Quantification of (A) blood urea nitrogen (BUN) and (B) creatinine levels in sham-treated and control (Ern1f/f + tamoxifen) as well as Ire1α-KO (Ern1f/f;Rosa26-CreERT2+ + tamoxifen) mice subjected to ischemia–reperfusion (IR). C Representative microscopic images of haematoxylin and eosin (H&E) staining of the renal cortex after treatment. Selected representative regions are enlarged and displayed in the corner. Dash lines outline damaged renal tubules (as characterized by tubular dilatation, tubule brush border loss, flattened epithelial cells or sloughing of cells). Scale bars: 200 μm. The histogram on the right shows the quantification of renal tubule damages. D Representative images of lipid peroxidation marker 4-HNE immunohistochemistry staining of renal cortex after IR treatment. Selected representative regions are enlarged and displayed at the corner. Scale bars: 200 μm. The histogram on the right shows the quantification of 4-HNE-positive tubules in the renal cortex. Data are presented as mean ± s.d. in (A, B) and the right panels of (C, D), with n = 5 (sham-treated), n = 13 (control + IR) and n = 15 (Ire1α-KO + IR) independent kidneys in the corresponding groups. P values were calculated from unpaired two-tailed Student’s t test. Source data are provided as a Source Data file.
