ArticleCell2021
Selective activation of PFKL suppresses the phagocytic oxidative burst.
Article in Cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 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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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.
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Who cites it
95 citing papers in PubMed, 152 citations in OpenAlex.
- The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026Review
- A covalent PFKL activator suppresses tumor growth.Nature chemical biology · 2026Article
- Copper homeostasis and cuproptosis: molecular mechanisms and therapeutic opportunities.Molecular biomedicine · 2026Review
- Engineered Neutrophils in Translational Medicine: Gene Editing, Nanotechnology, and AI-Driven Clinical Breakthroughs.Advanced healthcare materials · 2026Review
- Apical-out airway organoids as a pathophysiological model to study macrophage-mediated epithelial responses to microplastics.Materials today. Bio · 2026Article
- Lipid asymmetry disruption by XKR8 orchestrates neutrophil extracellular trap formation and inhibits fungal infection.Nature immunology · 2026Article
- Aryl hydrocarbon receptor impairs HK2-controlled flux of the hexosamine biosynthesis pathway to suppress NETosis in an N-glycosylation-dependent manner.Journal of advanced research · 2026Article
- Spatial and cellular composition of lung fibrosis induced by multi-walled carbon nanotubes.Journal of nanobiotechnology · 2026Article
- PFKM governs metabolic shifts throughout skeletal muscle differentiation.Nature metabolism · 2026Article
- Glycolysis enzymes and cellular lactylation in tumour.Clinical and translational medicine · 2026Review
- Association of remnant cholesterol and cholesterol, high-density lipoprotein, and glucose index with unfavorable outcomes after intravenous thrombolysis in acute ischemic stroke: a dual-center cohort study.Frontiers in immunology · 2026Article
- NEAT1 modulates neutrophil functions via glycolysis to restrain mucosal inflammation in ulcerative colitis.Frontiers in immunology · 2026Article
- Gasdermins in neurodegeneration: emerging mechanisms and therapeutic targets.Cell death & disease · 2025Review
- Dual clinical utility of cholesterol, high density lipoprotein, and glucose index: from advanced cardiovascular-kidney-metabolic syndrome pathogenesis to inflammatory-mediated mortality across early-transitional stages.Diabetology & metabolic syndrome · 2025Article
- Inhibiting the formation of neutrophil extracellular traps to prevent the recurrence of post-operative glioblastoma.Nature communications · 2025Article
- PFKP Lactylation Promotes the Ovarian Cancer Progression Through Targeting PTEN.Biochemical genetics · 2025Article
- Targeting PANoptosis: a promising therapeutic strategy for ALI/ARDS.Apoptosis : an international journal on programmed cell death · 2025Review
- mCell death & disease · 2025Article
- The noncanonical function of liver-type phosphofructokinase potentiates the efficacy of HDAC inhibitors in cancer.Signal transduction and targeted therapy · 2025Article
- Immunometabolism: crosstalk with tumor metabolism and implications for cancer immunotherapy.Molecular cancer · 2025Review
35 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
In neutrophils, nicotinamide adenine dinucleotide phosphate (NADPH) generated via the pentose phosphate pathway fuels NADPH oxidase NOX2 to produce reactive oxygen species for killing invading pathogens. However, excessive NOX2 activity can exacerbate inflammation, as in acute respiratory distress syndrome (ARDS). Here, we use two unbiased chemical proteomic strategies to show that small-molecule LDC7559, or a more potent designed analog NA-11, inhibits the NOX2-dependent oxidative burst in neutrophils by activating the glycolytic enzyme phosphofructokinase-1 liver type (PFKL) and dampening flux through the pentose phosphate pathway. Accordingly, neutrophils treated with NA-11 had reduced NOX2-dependent outputs, including neutrophil cell death (NETosis) and tissue damage. A high-resolution structure of PFKL confirmed binding of NA-11 to the AMP/ADP allosteric activation site and explained why NA-11 failed to agonize phosphofructokinase-1 platelet type (PFKP) or muscle type (PFKM). Thus, NA-11 represents a tool for selective activation of PFKL, the main phosphofructokinase-1 isoform expressed in immune cells.
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What OpenQuestion holds
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.