ArticleScience translational medicine2018
Inhibition of IP6K1 suppresses neutrophil-mediated pulmonary damage in bacterial pneumonia.
Article in Science translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
33 citing papers in PubMed, 50 citations in OpenAlex.
- Inositol pyrophosphate kinases in health and disease.FEBS letters · 2026Review
- Exercise suppresses IP6K3 to modulate BCAA metabolism and ferroptosis in MASLD.Cellular & molecular biology letters · 2026Article
- Inhibition of IP6K1 suppresses NPA formation via platelet short-chain polyphosphate polymers in necrotizing enterocolitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The inositol pyrophosphate 5-InsPThe Journal of biological chemistry · 2026Article
- Neutrophil-derived vesicles control complement activation to facilitate inflammation resolution.Cell · 2025Article
- A pan-immune panorama of bacterial pneumonia revealed by a large-scale single-cell transcriptome atlas.Signal transduction and targeted therapy · 2025Article
- Knockout Mice as an Experimental Model to Study the Biology of Inositol Pyrophosphates.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Experimental animal models of acute respiratory distress syndrome: one-hit and two-hit establishment application.Frontiers in immunology · 2025Review
- Balancing immune response: SHP1 controls neutrophil activation in inflamed lungs.The Journal of clinical investigation · 2024Article
- S1PR3 inhibition protects against LPS-induced ARDS by inhibiting NF-κB and improving mitochondrial oxidative phosphorylation.Journal of translational medicine · 2024Article
- Insights into the roles of inositol hexakisphosphate kinase 1 (IP6K1) in mammalian cellular processes.The Journal of biological chemistry · 2024Review
- Exosomal secreted SCIMP regulates communication between macrophages and neutrophils in pneumonia.Nature communications · 2024Article
- Distinctive features and prognostic utility of neutrophil in severe patients withFrontiers in cellular and infection microbiology · 2024Article
- Fragment-Based Screening Identifies New Quinazolinone-Based Inositol Hexakisphosphate Kinase (IP6K) Inhibitors.ACS medicinal chemistry letters · 2023Article
- The Role of Inositol Hexakisphosphate Kinase in the Central Nervous System.Biomolecules · 2023Review
- Role of neutrophils in different stages of atherosclerosis.Innate immunity · 2023Review
- The IP6K Inhibitor LI-2242 Ameliorates Diet-Induced Obesity, Hyperglycemia, and Hepatic Steatosis in Mice by Improving Cell Metabolism and Insulin Signaling.Biomolecules · 2023Article
- Immunomodulation of neutrophil granulocyte functions by bacterial polyphosphates.European journal of immunology · 2023Article
- Gene signature of circulating platelet-bound neutrophils is associated with poor prognosis in cancer patients.International journal of cancer · 2022Article
- Development of Novel IP6K Inhibitors for the Treatment of Obesity and Obesity-Induced Metabolic Dysfunctions.Journal of medicinal chemistry · 2022Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
The significance of developing host-modulating personalized therapies to counteract the growing threat of antimicrobial resistance is well-recognized because such resistance cannot be overcome using microbe-centered strategies alone. Immune host defenses must be finely controlled during infection to balance pathogen clearance with unwanted inflammation-induced tissue damage. Thus, an ideal antimicrobial treatment would enhance bactericidal activity while preventing neutrophilic inflammation, which can induce tissue damage. We report that disrupting the inositol hexakisphosphate kinase 1 (
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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.