ArticlemBio2023
MLKL-Driven Inflammasome Activation and Caspase-8 Mediate Inflammatory Cell Death in Influenza A Virus Infection.
Article in mBio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 43 citations in OpenAlex.
- Biological consequences of Z-nucleic acid sensing by ZBP1 and ADAR1.RNA biology · 2026Review
- Programmed cell death in metabolic syndrome: From molecular mechanisms to therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Degradation of ACSL3 by influenza A virus shifts unfolded protein response from antiviral defense to viral evasion.Virologica Sinica · 2026Article
- Pyroptosis in cerebral ischemia‑reperfusion injury: Molecular mechanisms and therapeutic implications (Review).Molecular medicine reports · 2026Review
- Article
- RIPK3 Orchestrates Scar-Associated Macrophage Dysfunction to Drive Pulmonary Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Immune molecular mechanisms of PANoptosis in sepsis-induced acute kidney injury.Inflammation and regeneration · 2026Review
- Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers.Apoptosis : an international journal on programmed cell death · 2026Review
- Immune Aging as a Failure of Programmed Cell Death Coordination.International journal of molecular sciences · 2026Review
- Epigenetic regulation of PANoptosis: DNA methylation, histone modifications and non-coding RNAs.EXCLI journal · 2026Review
- Orchestrating immunopathology: the spectrum of programmed cell death pathways co-opted by influenza a virus in pulmonary immunity.Frontiers in immunology · 2026Review
- Post-translational modification networks as master regulators of influenza virus replication, host adaptation, and immune evasion.Frontiers in immunology · 2026Review
- Necroptotic cell death consequences and disease relevance.Nature immunology · 2025Review
- Caspase cleavage of Kaposi sarcoma-associated herpesvirus proteins: a role for K5 in preventing caspase-mediated cell death during lytic replication.Journal of virology · 2025Article
- Ninjurin-1 mediates cell lysis and detrimental inflammation of PANoptosis during influenza A virus infection.Signal transduction and targeted therapy · 2025Article
- Establishment of rat model for aspiration pneumonia and potential mechanisms.Animal models and experimental medicine · 2025Article
- ZBP1-driven cell death in severe influenza.Trends in microbiology · 2025Review
- Article
- Article
- Fibroblast heterogeneity and its role in generating protective immunity in the secondary lymphoid organs.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Influenza A virus (IAV) triggers multiple programmed cell death pathways, including MLKL-dependent necroptosis, caspase-8-dependent apoptosis, and caspase-1-dependent pyroptosis in myeloid cells. All three pathways share common upstream regulators, namely, ZBP1 and RIPK3. Yet, the molecular mechanism underlying IAV-induced inflammasome activation remains unclear. Here, we demonstrate that MLKL promotes inflammasome activation and IL-1β processing in IAV-infected macrophages. MLKL drives NLRP3 inflammasome activation through potassium efflux. In the absence of the MLKL-inflammasome axis, caspase-8 coordinates the maturation and secretion of IL-1β. MLKL alone is dispensable for host inflammatory responses to IAV in vivo. Taken together, MLKL and caspase-8 serve as redundant mechanisms by which to drive an inflammatory form of cell death in response to an IAV infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.