Journal: Frontiers in Pharmacology

Article Title: Integrated transcriptomics identifies ER stress–associated apoptosis in post-resuscitation AKI and supports early Dl-3-n-butylphthalide–associated renoprotection in a porcine TCA model

doi: 10.3389/fphar.2026.1841271

Figure Lengend Snippet: Differential expression, ERS/UPR-associated pathways, and PERK–ATF4–CHOP axis-gene signals from bulk microarray data. (A) Volcano plot of IRI versus Sham shows widespread transcriptional remodeling, with multiple stress- and injury-related genes among the prominently altered signals. (B) Hallmark GSEA dot plot indicates enrichment of the Hallmark Unfolded Protein Response and Hallmark Apoptosis pathways, accompanied by activation of injury-response pathways such as Hypoxia, TNFα/NF-κB, inflammatory response, and p53 signaling. (C) ssGSEA heatmap at the sample level shows condition-related increases in UPR_total and Apoptosis activity in the IRI group, with branch-specific variation across UPR-related scores. (D) Heatmap of PERK–ATF4–CHOP axis genes shows increased z-score expression of Atf4 and Ddit3/CHOP in IRI samples relative to Sham samples.

Article Snippet: Among these branches, PERK–ATF4–CHOP signaling can shift from adaptive proteostasis regulation toward pro-apoptotic signaling under severe or sustained stress.

Techniques: Quantitative Proteomics, Microarray, Activation Assay, Activity Assay, Expressing

Journal: Frontiers in Pharmacology

Article Title: Integrated transcriptomics identifies ER stress–associated apoptosis in post-resuscitation AKI and supports early Dl-3-n-butylphthalide–associated renoprotection in a porcine TCA model

doi: 10.3389/fphar.2026.1841271

Figure Lengend Snippet: PT pseudo-bulk pathway enrichment and PERK–ATF4–CHOP axis-gene signals (A) Hallmark GSEA dot plot from PT pseudo-bulk analysis highlights Unfolded Protein Response and Apoptosis among the significantly altered pathways in the Sham versus IRI_12 h contrast. Because the contrast direction is Sham versus IRI_12h, negative NES values indicate enrichment toward the IRI_12 h condition. (B) PT pseudo-bulk volcano plot shows extensive transcriptional remodeling, with ERS/UPR- and apoptosis-related genes represented among the significantly altered signals. (C) Heatmap of axis-gene logFC across key PT pseudo-bulk contrasts shows coordinated changes in core UPR mediators, including Hspa5, Eif2ak3/PERK, Atf4, Ddit3/CHOP, Ern1/Xbp1, and Atf6, together with apoptosis-related genes including Bax, Bak1, Casp3/8/9, and Bcl2l1. Stars indicate FDR <0.05. (D) Bar plots of representative PT pseudo-bulk axis genes show contrast-level changes in PERK–ATF4–CHOP branch components, UPR-related mediators, and apoptosis-related effectors, including Eif2ak3/PERK, Atf4, Ddit3/CHOP, Hspa5, Ern1, Xbp1, Bax, and Bcl2l1. Stars indicate FDR <0.05.

Article Snippet: Among these branches, PERK–ATF4–CHOP signaling can shift from adaptive proteostasis regulation toward pro-apoptotic signaling under severe or sustained stress.

Techniques:

Journal: Cell Reports Medicine

Article Title: Taxane chemotherapy promotes response to TIM-3 checkpoint blockade via STING-mediated ER stress and HMGB1 secretion

doi: 10.1016/j.xcrm.2026.102788

Figure Lengend Snippet: Taxanes induce STING-dependent ER stress and HMGB1 exocytosis (A) ER Tracker Blue-White fluorescence in control, Cgas -deficient, or Sting- deficient PyMT-B6 cells pretreated with NAC for 1 h prior to treatment with DTX or tunicamycin (Tuni). Data reflect the mean ± SD of three biological replicates, with significance determined by one-way ANOVA with Sidak’s test for multiple comparisons, shown as ∗ p < 0.05 and ∗∗∗ p < 0.001. One of three independent experiments shown. (B) Western blot of ER stress/UPR markers present in PyMT-B6 cells 16 h after indicated treatment. Vinculin was used as loading control. Molecular weights in kDa are shown to the left. One of three independent experiments shown. (C) Extracellular flow cytometric detection of LAMP1 on control, Cgas -deficient, or Sting- deficient PyMT-B6 cells pretreated with NAC, IRE1α inhibitor MKC8866, or PERK inhibitor AMG44 for 1 h prior to treatment with DTX. Data reflect the mean ± SD of three biological replicates, with significance determined by one-way ANOVA with Sidak’s test for multiple comparisons, shown as ∗∗∗ p < 0.001. One of three independent experiments shown. (D and E) Flow cytometric detection of extracellular LAMP1 (D) or intracellular HMGB1 (E) in PyMT-B6 cells 24 h post-calcium chelation with a 1-h pretreatment of BAPTA, +/− DTX treatment. HMGB1 percent positivity is shown in red on the flow plots (right). Data reflect the MFI ±SD of three biological replicates, with significance determined by one-way ANOVA with Sidak’s test for multiple comparisons, shown as ∗∗∗ p < 0.001. One representative experiment of three shown. (F) Flow cytometric detection of intracellular HMGB1 in control or Cgas- and Sting- deficient PyMT-B6 cells pretreated with IRE1α (MKC8866) or PERK inhibitor (AMG44) for 1 h prior to treatment with DTX. Data reflect the mean ± SD of three biological replicates, with significance determined by one-way ANOVA with Sidak’s test for multiple comparisons, shown as ∗∗∗ p < 0.001.

Article Snippet: AMG PERK 44, PERK Inhibitor , MedChemExpress , Cat# HY-12661 A.

Techniques: Fluorescence, Control, Western Blot