ArticleViruses2023
ZBP1 Drives IAV-Induced NLRP3 Inflammasome Activation and Lytic Cell Death, PANoptosis, Independent of the Necroptosis Executioner MLKL.
Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 46 citations in OpenAlex.
- The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.Cellular & molecular immunology · 2026Review
- PANoptosis in life and death across cell types: From innate immunity to therapeutic implications.Cell chemical biology · 2026Review
- Pseudorabies virus infection induces IRF1-dependent PANoptosis to provoke the excessive release of HMGB1 and IL-1β.Communications biology · 2026Article
- [Role of programmed cell death in platinum resistance in ovarian cancer].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Defining critical roles for ZBP1 in PANoptosis utilizing a novel genetic tool for disease modeling and therapeutic development.bioRxiv : the preprint server for biology · 2026Article
- Immune molecular mechanisms of PANoptosis in sepsis-induced acute kidney injury.Inflammation and regeneration · 2026Review
- Rift Valley fever virus activates multiple cell death pathways in neurons.Journal of virology · 2026Article
- Identification and validation of PANoptosis-related genes in ankylosing spondylitis.BMC medical genomics · 2026Article
- PANoptosis in neurological disorders: from inflammatory cell death mechanisms to neuroprotective strategies.Frontiers in neuroscience · 2026Review
- Mitochondrial dysfunction and PANoptosis-related signaling in acute central nervous system injuries: mechanistic convergence and therapeutic opportunities.Frontiers in molecular neuroscience · 2026Review
- ZBP1 as a dynamic monitor of viral replication: implications for therapeutic strategies.Frontiers in cellular and infection microbiology · 2026Review
- Convergent hub pathways targeted by IAV, SARS-CoV-2, and RSV in type II alveolar epithelial cells: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Emerging role of PANoptosis in pathogen infection and systemic diseases.Cell biology and toxicology · 2025Review
- Emerging Insights into the Interplay Between PANoptosis and Autophagy in Immune Regulation and Immune-Mediated Inflammatory Diseases.Medical sciences (Basel, Switzerland) · 2025Review
- PANoptosis: potential new targets and therapeutic prospects in digestive diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025Review
- Three decades of caspases and RIPKs in life and death.Human molecular genetics · 2025Review
- Pyroptosis in Respiratory Virus Infections: A Narrative Review of Mechanisms, Pathophysiology, and Potential Therapeutic Interventions.Microorganisms · 2025Review
- PANoptosis-mediated mechanisms underlying AST elevation in Talaromyces marneffei infection.PLoS neglected tropical diseases · 2025Article
- Heme Unleashed: NLRP12 Orchestrates PANoptosis in a Symphony of Cell Fate.Cell biochemistry and biophysics · 2025Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Influenza A virus (IAV) continues to pose a significant global health threat, causing severe respiratory infections that result in substantial annual morbidity and mortality. Recent research highlights the pivotal role of innate immunity, cell death, and inflammation in exacerbating the severity of respiratory viral diseases. One key molecule in this process is ZBP1, a well-recognized innate immune sensor for IAV infection. Upon activation, ZBP1 triggers the formation of a PANoptosome complex containing ASC, caspase-8, and RIPK3, among other molecules, leading to inflammatory cell death, PANoptosis, and NLRP3 inflammasome activation for the maturation of IL-1β and IL-18. However, the role for other molecules in this process requires further evaluation. In this study, we investigated the role of MLKL in regulating IAV-induced cell death and NLRP3 inflammasome activation. Our data indicate IAV induced inflammatory cell death through the ZBP1-PANoptosome, where caspases and RIPKs serve as core components. However, IAV-induced lytic cell death was only partially dependent on RIPK3 at later timepoints and was fully independent of MLKL throughout all timepoints tested. Additionally, NLRP3 inflammasome activation was unaffected in MLKL-deficient cells, establishing that MLKL and MLKL-dependent necroptosis do not act upstream of NLRP3 inflammasome activation, IL-1β maturation, and lytic cell death during 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.