ArticleVirulence2022
AP-1 signaling pathway promotes pro-IL-1β transcription to facilitate NLRP3 inflammasome activation upon influenza A virus infection.
Article in Virulence, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 62 citations in OpenAlex.
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Mechanisms and Predisposing Conditions for Statin-Induced New-Onset Type 2 Diabetes Mellitus: A Paradox Relative to Their Pleiotropic Metabolic Effects.Endocrinology, diabetes & metabolism · 2026Review
- Differential Host Gene Expression Associated with Non-Research square · 2026Article
- PANoptosis as a Therapeutic Target for COVID-19.Current microbiology · 2026Review
- TRIM5 integrates hypoglycemic stress and influenza infection.Nature communications · 2026Article
- Integrated network pharmacology, transcriptomics and experimental validation to explore mechanisms of Wenyang Jiedu Granule on IAV-induced pneumonia.Chinese herbal medicines · 2026Article
- Dual-mechanistic regulation of podocyte pyroptosis in lupus nephritis by the AP-1 complex: transcriptional activation of NLRP3 and lactate-mediated ubiquitination inhibition.Cell communication and signaling : CCS · 2026Article
- Beyond pathogens: a narrative review of the immunological nexus of damage-associated molecular patterns and inflammasome activation in sterile AECOPD.Frontiers in immunology · 2026Review
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
- Curcumol alleviates cardiac and cerebral injury caused by encephalomyocarditis virus (EMCV) in Kunming mice via suppressing NF-κB/NLRP3 inflammasome pathway.Frontiers in pharmacology · 2026Article
- NF-κB-dependent and independent inflammatory responses during acute HIV-1 infection in a model of human microglia.Frontiers in immunology · 2026Article
- CD63Frontiers in cellular and infection microbiology · 2026Article
- The cellular activating protein-1 cFos regulates influenza A virus replication.The Journal of general virology · 2026Article
- Research advances on NLRP3 inflammasomes in organ transplantation.Frontiers in immunology · 2026Review
- Inflammasomes and pyroptosis in cancer: mechanisms and therapeutic advances.Journal of hematology & oncology · 2025Review
- Prenatal alcohol exposure promotes nerve injury-induced pathological pain following morphine treatment via NLRP3-mediated peripheral and central proinflammatory immune actions.Brain, behavior, and immunity · 2025Article
- Integrated miRNA-mRNA Atlas Reveals Temperature-Graded Brain Neuroendocrine Adaptation to Cold Stress in Silvery Pomfret (Biology · 2025Article
- An advanced network pharmacology investigation of Shufeng Jiedu formula in the treatment for respiratory tract infection based on LC-MS, data mining, molecular docking, and molecular dynamic simulation.Briefings in bioinformatics · 2025Article
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- Hesperetin Inhibits Porcine Reproductive and Respiratory Syndrome Virus Replication by Downregulating the P38/JUN/FOS Pathway In Vitro.Microorganisms · 2025Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NLRP3 inflammasome mainly controls interleukin-1β (IL-1β) secretion, leading to cell death called pyroptosis constituting a major antiviral host defense and inflammatory diseases upon viral infection. The RAF-MEK1/2-ERK1/2 cascade and downstream c-Jun/Fos and Activator protein-1 (AP1) signaling pathway control the degree of inflammatory response. Influenza A virus (IAV) infection is known to stimulate NLRP3 inflammasome activation and inflammatory responses. Nevertheless, the detailed mechanism by which IAV induces NLRP3 inflammasome activation involved in transcription of pro-IL-1β mRNA remains elusive. In our study, we found that IAV infection promotes pro-IL-1β mRNA transcription and activates NLRP3 inflammasome. Detailed studies reveal that type I interferon (IFN-α/IFN-β) as well as U0126 (a selective inhibitor of MEK-1 and MEK-2) typically inhibit IAV-mediated NLRP3 inflammasome activation via downregulating pro-IL-1β mRNA. Moreover, knock-down of c-Jun decreases pro-IL-1β mRNA and inhibits NLRP3 inflammasome activation upon IAV infection. Overall, the findings uncover that AP-1 signaling pathway promotes NLRP3 inflammasome activation upon IAV infection, which provides a new idea for the therapy of NLRP3 inflammasome-associated inflammatory diseases.
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