ArticleCells2022
Interferon-γ Preferentially Promotes Necroptosis of Lung Epithelial Cells by Upregulating MLKL.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- Necroptosis and the RIPK1-RIPK3-MLKL pathway in chronic kidney disease: mechanisms, crosstalk, and therapeutic opportunities.Renal failure · 2026Review
- Inflammatory cytokines induce new cancer dependencies.Nature genetics · 2026Article
- Orphan Nuclear Receptors expression and function in breast cancer cells: oncogenic action of the NR2F6 receptor.Cell communication and signaling : CCS · 2026Article
- Regulatory complexity and therapeutic targeting of the necroptosis network.Frontiers in immunology · 2026Review
- Podocyte-specific acid sphingomyelinase overexpression promotes gasdermin D dependent pyroptosis by impairing autophagic flux during obesity.Frontiers in physiology · 2026Article
- Development of delayed pulmonary toxicities and transcriptional changes in pre-existing interstitial lung disease mice after partial thoracic irradiation.Radiation oncology (London, England) · 2025Article
- A narrative review on lung injury: mechanisms, biomarkers, and monitoring.Critical care (London, England) · 2024Review
- Targeting necroptosis: a promising avenue for respiratory disease treatment.Cell communication and signaling : CCS · 2024Review
- Runx3 Regulates CD8International journal of molecular sciences · 2024Article
- IE1 of Human Cytomegalovirus Inhibits Necroptotic Cell Death via Direct and Indirect Modulation of the Necrosome Complex.Viruses · 2024Article
- Necroptosis does not drive disease pathogenesis in a mouse infective model of SARS-CoV-2 in vivo.Cell death & disease · 2024Article
- KAE ameliorates LPS-mediated acute lung injury by inhibiting PANoptosis through the intracellular DNA-cGAS-STING axis.Frontiers in pharmacology · 2024Article
- A mammalian lung's immune system minimizes tissue damage by initiating five major sequential phases of defense.Clinical and experimental medicine · 2023Review
- The Many Faces of MLKL, the Executor of Necroptosis.International journal of molecular sciences · 2023Review
- Involvement of Pore Formation and Osmotic Lysis in the Rapid Killing of Gamma Interferon-Pretreated C166 Endothelial Cells byTropical medicine and infectious disease · 2022Article
- Cephalosporins-induced intestinal dysbiosis exacerbated pulmonary endothelial barrier disruption in streptococcus pneumoniae-infected mice.Frontiers in cellular and infection microbiology · 2022Article
- Lignans fromEvidence-based complementary and alternative medicine : eCAM · 2022Article
- Inducible general knockout of Runx3 profoundly reduces pulmonary cytotoxic CD8Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Necroptosis, a form of programmed lytic cell death, has emerged as a driving factor in the pathogenesis of acute lung injury (ALI). As ALI is often associated with a cytokine storm, we determined whether pro-inflammatory cytokines modulate the susceptibility of lung cells to necroptosis and which mediators dominate to control necroptosis. In this study, we pretreated/primed mouse primary lung epithelial and endothelial cells with various inflammatory mediators and assessed cell type-dependent responses to different necroptosis inducers and their underlying mechanisms. We found that interferon-γ (IFNγ) as low as 1 ng/mL preferentially promoted necroptosis and accelerated the release of damage-associated molecular patterns from primary alveolar and airway epithelial cells but not lung microvascular endothelial cells. Type-I IFNα was about fifty-fold less effective than IFNγ. Conversely, TNFα or agonists of Toll-like receptor-3 (TLR3), TLR4, TLR7 and TLR9 had a minor effect. The enhanced necroptosis in IFNγ-activated lung epithelial cells was dependent on IFNγ signaling and receptor-interacting protein kinase-3. We further showed that necroptosis effector mixed lineage kinase domain-like protein (MLKL) was predominantly induced by IFNγ, contributing to the enhanced necroptosis in lung epithelial cells. Collectively, our findings indicate that IFNγ is a potent enhancer of lung epithelial cell susceptibility to necroptosis.
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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.