Journal: Materials Today Bio

Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation

doi: 10.1016/j.mtbio.2026.102974

Figure Lengend Snippet: COPN mitigates retinal ischemia‒reperfusion injury by suppressing the cGAS–STING–TBK1 signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: The following primary antibodies were used: Drp1 (CST, #8570, 1:1000, ∼80 kDa), Fis1 (Proteintech, 10956-1-AP, 1:1000, ∼17 kDa), Mfn1 (Abcam, ab104274, 1:1000, ∼84 kDa), Mfn2 (CST, #9482, 1:1000, ∼86 kDa), Opa1 (CST, #80471, 1:1000, ∼100–120 kDa), Pink1 (CST, #6946, 1:1000, ∼63 kDa), cGAS (CST, #15102, 1:1000, ∼60 kDa), STING (CST, #13647, 1:1000, ∼42–45 kDa), TBK1 (CST, #3013, 1:1000, ∼84 kDa), p-TBK1 (CST, #5483, 1:1000, ∼84 kDa), COX IV (Abcam, ab14744, 1:2000, ∼17 kDa), β-actin (Proteintech, 66009-1-Ig, 1:5000, ∼43 kDa), and GAPDH (Proteintech, 60004-1-Ig, 1:5000, After washing, the membranes were incubated with HRP-conjugated secondary antibodies (goat anti-rabbit or goat anti-mouse IgG, CST, 1:5000) for 1 h at room temperature.

Techniques: Quantitative Proteomics, Control, Activation Assay, Phospho-proteomics, Disruption, Western Blot

Journal: Materials Today Bio

Article Title: A dual-responsive CO-releasing nanogel ameliorates retinal ischemia–reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation

doi: 10.1016/j.mtbio.2026.102974

Figure Lengend Snippet: COPN mitigates retinal ischemia‒reperfusion injury by suppressing the cGAS–STING–TBK1 signaling axis. a , Heatmap illustrating the differential expression of key genes involved in mitochondrial function, apoptosis, and inflammatory responses between OHT-treated and control retinas. b , Gene Ontology (GO) enrichment analysis highlighting significantly enriched biological processes and molecular functions, including the mitochondrial stress response, cGAS-STING complex activation, and neuroinflammation. c , Volcano plot depicting significantly differentially expressed genes (DEGs) between the OHT and control groups, with upregulated genes in red and downregulated genes in blue. d , KEGG pathway enrichment analysis revealed significant activation of oxidative phosphorylation disruption, apoptosis, inflammation, and notably the cGAS‒STING signaling pathway in retinal ischemia. e , RT‒qPCR quantification of key components of the cGAS‒STING pathway (cGAS, STING, TBK1, IRF3, and caspase-3) in the retinas of mice after different treatments. f–g , Western blot analyses of cGAS-STING pathway-related proteins (cGAS, STING, p-STING, TBK1, p-TBK1, IRF3, p-IRF3, and cleaved caspase-3) under (f) OGD/R stress in R28 cells and (g) retinal tissues from OHT mice. ∗∗∗∗ P < 0.0001. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: The following primary antibodies were used: Drp1 (CST, #8570, 1:1000, ∼80 kDa), Fis1 (Proteintech, 10956-1-AP, 1:1000, ∼17 kDa), Mfn1 (Abcam, ab104274, 1:1000, ∼84 kDa), Mfn2 (CST, #9482, 1:1000, ∼86 kDa), Opa1 (CST, #80471, 1:1000, ∼100–120 kDa), Pink1 (CST, #6946, 1:1000, ∼63 kDa), cGAS (CST, #15102, 1:1000, ∼60 kDa), STING (CST, #13647, 1:1000, ∼42–45 kDa), TBK1 (CST, #3013, 1:1000, ∼84 kDa), p-TBK1 (CST, #5483, 1:1000, ∼84 kDa), COX IV (Abcam, ab14744, 1:2000, ∼17 kDa), β-actin (Proteintech, 66009-1-Ig, 1:5000, ∼43 kDa), and GAPDH (Proteintech, 60004-1-Ig, 1:5000, After washing, the membranes were incubated with HRP-conjugated secondary antibodies (goat anti-rabbit or goat anti-mouse IgG, CST, 1:5000) for 1 h at room temperature.

Techniques: Quantitative Proteomics, Control, Activation Assay, Phospho-proteomics, Disruption, Western Blot

Journal: Nature Communications

Article Title: IRAK2 deficiency causes immune dysregulation through defective Myddosome assembly and enhanced interferon responses

doi: 10.1038/s41467-026-73383-8

Figure Lengend Snippet: a Immunoblotting of IRAK2 -knockout (KO) THP-1 cells reconstituted with control empty vector (EV), IRAK2-WT, or IRAK2-∆ex2 after stimulation with 10 ng/mL LPS for indicated times. b Quantitative PCR (qPCR) of IFNB1 expression in cells described in ( a ). c Immunoblotting of IRF3, IKKε, and TBK1 phosphorylation in reconstituted THP-1 cells stimulated with LPS (10 ng/mL, 2 h) with or without pretreatment with a TIRAP inhibitor (10 μM, 2 h) or a TRIF inhibitor (10 μM, 2 h). d qPCR of IFNB1 expression in cells described in ( c ). LPS + + indicates pretreatment with both inhibitors. e Immunoblotting of IRF3 and TBK1 phosphorylation in reconstituted THP-1 cells stimulated with LPS (10 ng/mL, 2 h) after TICAM1 (TRIF) knockdown with two independent siRNAs (siRNA#1 and siRNA#2); non-targeting siRNA (siRNA#C) served as control. f qPCR of IFNB1 expression in cells described in ( e ). g Immunoblotting of IRF3 phosphorylation in reconstituted THP-1 cells stimulated with LPS (10 ng/mL, 2 h) with or without pretreatment with a TBK1/IKKε inhibitor (1 μM, 30 min) or a TAK1 inhibitor (100 nM, 30 min). h qPCR of IFNB1 expression in cells described in ( g ). i RNA sequencing of IFN pathway in peripheral blood mononuclear cells (PBMCs) from P4, P11, and three unaffected controls at baseline. P4_Bari and P11_Bari indicate Baricitinib-treated PBMCs (0.5 μM, 12 h). Freshly isolated PBMCs were sequenced with batch correction. Each sample was processed in two technical repeats. Sample were collected from P4 in April 2023 (P4_1), November 2023 (P4_2), and November 2024 (P4_3 and P4_Bari), and from P11 in May 2025 (P11_1) and June 2025 (P11_2 and P11_Bari). j Immunoblotting of the effect of Baricitinib (0.5 μM, 12 h) on THP-1 cells. k qPCR of IFIT1 and IFIT3 expression in cells described in ( j ). Two-way ANOVA with Šídák’s multiple-comparisons test was applied. Bars represent mean of n = 5 ± SEM (biological replicates). For b, d, f , h , two-way ANOVA with Tukey’s multiple-comparisons test was applied, and bars represent mean of n = 5 ± SEM (biological replicates).

Article Snippet: PMA-differentiated THP-1 cell lines and PBMCs were treated with 0.5 μM Baricitinib (LY3009104, MCE) for 12 h. PMA-differentiated THP-1 cells were pretreated with TIRAP inhibitor (NBP2-29331, Novus; 10 μM for 2 h), TRIF inhibitor (HY-P2565, MCE; 10 μM for 2 h), TBK1/IKKε inhibitor (HY-12453, MCE; 1 μM for 30 min), or TAK1 inhibitor (HY-12686, MCE; 100 nM for 30 min) prior to LPS stimulation.

Techniques: Western Blot, Knock-Out, Control, Plasmid Preparation, Real-time Polymerase Chain Reaction, Expressing, Phospho-proteomics, Knockdown, RNA Sequencing, Isolation