Fig 2: Inhibition of IDH1 ameliorates ox-LDL-induced ferroptosis. (A) The levels of GSH. (B) The level of iron content. (C) The total content of LPO. (D) Cell survival determined by CCK-8. (E) The brightfield images showing dead cells (Scale bars = 50 µm). ## p < 0.01 vs. control group; * p < 0.05, ** p < 0.01 vs. ox-LDL-treated group; NS vs. ox-LDL and si-IDH1 treatment group. & p < 0.05, && p < 0.01 vs. ox-LDL and Fer-1 treatment group. NS, not significant. Data are presented as mean ± SD.

Fig 3: IHC staining in tumor-bearing mouse. (A) ki-67. (B) IDH1. (C) HIF-1α. (D) HIF-2α. (E) VEGF. (F) TGF-α.

Fig 4: High-throughput profiling of lncRNA–protein interactions using HuProt arrays. (A) Scheme of HuProt array-based assay to reveal lncRNA-binding proteins in an unbiased manner. And the results of HuProt array screens are summarized and shown below. (B) A typical example of the results from HuProt arrays. Each microarray was divided into 48 blocks (bottom). Each block contains 800 protein spots. Controls, including negative controls (histone H1 and H4, buffer, GST and BSA) and the positive control IgG, are printed in the last row of each block as indicated, and tested proteins are printed in duplicate. In this example, the Cy5-labeled RNA probe selectively interacts with proteins such as YBX1, MTHFD1, SLC39A1, IDH1 and mutant IDH1 (S307A) (top).

Fig 5: Inhibition of IDH1 ameliorates ox-LDL-induced macrophage apoptosis. (A,B) Apoptosis of RAW264.7 cells in different groups was examined via flow cytometry. (C) JASPAR-predicted NRF2 transcription factor binding sites. (D) Nrf2 and IDH1 potential binding sites. (E) Relative enrichment of IDH1, detected by ChIP. ## p < 0.01 vs. control group; ** p < 0.01 vs. ox-LDL-treated group; NS vs. ox-LDL and si-IDH1 treatment group. && p < 0.01 vs. ox-LDL and Fer-1 treatment group. NS, not significant. Data are presented as mean ± SD.