Curcuminoids amplify host innate antiviral immunity via the CRYAB‐RBM26 axis in viral infection
Rattachement africain : cn, ru, th. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Abstract Curcuminoids, including curcumin (CUR) and demethoxycurcumin (DMC), are known for their antiviral properties, but their underlying antiviral targets remain unclear, and the relationship between curcuminoids and the type I interferon (IFN‐I) signaling pathway has not been fully elucidated. Here, we explored the regulatory effects of DMC and CUR on the IFN‐I pathway in an EV‐D68‐infected murine model and employed multiomics analysis to identify key drug targets and their interaction networks. FTIR analysis indicated that DMC has better physicochemical stability than CUR, exhibiting greater stability under changes in light, temperature, and pH. In both in vitro and neonatal mouse models, DMC and CUR effectively inhibited EV‐D68 replication by suppressing viral 2A gene expression and the release of proinflammatory cytokines. Both compounds upregulated the molecular chaperone CRYAB (αB‐crystallin), which translocates to the nucleus and acts as a central regulator of host metabolism and antiviral immunity during EV‐D68 infection. Further multiomics analyses revealed that CRYAB overexpression inhibited purine metabolism and upregulated interferon‐stimulated genes. Proteomic profiling identified RBM26 as a key CRYAB‐interacting target. CRYAB stabilizes RBM26 by inhibiting virus‐induced ubiquitination, which leads to enhanced IFN‐I responses. DMC and CUR activated the mtDNA‐cGAS‐STING pathway via RBM26, stimulating downstream signaling and antiviral effects. RBM26 reconstitution altered the splicing of cytidine/uridine monophosphate kinase 2 ( CMPK2 ), resulting in increased nucleotide turnover and reduced cytidine levels, impairing viral replication. DMC/CUR treatment or CRYAB overexpression similarly reduced intracellular cytidine and uridine levels, increasing antiviral activity. Additionally, DMC/CUR restored mtDNA levels suppressed by EV‐D68 infection in an RBM26‐dependent manner, stimulating cGAS‐mediated cGAMP production and activating the STING‐TBK1‐IRF3 axis. These findings not only clarify the molecular mechanisms underlying the antiviral effects of curcuminoids but also highlight their therapeutic potential as host‐directed antiviral agents.
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Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Curcuminoids amplify host innate antiviral immunity via the CRYAB‐RBM26 axis in viral infection
- Date Crossref
- 01/02/2026
- Éditeur
- Wiley
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Dalian Medical University pays non établi dans la noticeUniversité ou école supérieure
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Second Affiliated Hospital of Chongqing Medical University pays non établi dans la noticeÉtablissement de santé
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Chongqing Emergency Medical Center pays non établi dans la noticeÉtablissement de santé
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Jinfeng Laboratory pays non établi dans la noticeStructure de recherche
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Chongqing Medical University Pathogen Biology and Immunology Laboratory pays non établi dans la noticeUniversité ou école supérieure
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Institute of Chemical Industry of Forest Products pays non établi dans la noticeStructure de recherche
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Guiyang Medical University pays non établi dans la noticeUniversité ou école supérieure
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Institute of Cytology pays non établi dans la noticeStructure de recherche
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Hubei University of Chinese Medicine pays non établi dans la noticeUniversité ou école supérieure
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Ministry of Education pays non établi dans la noticeOrganisme public
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Institute of Panvascular Biology pays non établi dans la noticeStructure de recherche
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National Key Laboratory for Development and Utilization of Forest Food Resources pays non établi dans la noticeStructure de recherche
Dalian Medical University, Second Affiliated Hospital of Chongqing Medical University et Chongqing Emergency Medical Center, avec 9 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.