Trial reportThe Journal of biological chemistry2014
Mitochondria regulate neutrophil activation by generating ATP for autocrine purinergic signaling.
Trial report in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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
91 citing papers in PubMed, 143 citations in OpenAlex.
- Innate Immune Function of Neutrophil Cytoplasts Generated Post-Vital NETosis.Research square · 2026Article
- Metabolic Control of Immunity-Unveiling Neutrophil Mechanisms.Advances in experimental medicine and biology · 2026Review
- Neutrophil-based delivery platforms: from natural mechanisms to engineered therapeutics.Theranostics · 2026Review
- Targeting proBDNF in neutrophil subsets: Sepsis biomarker discovery and insights into mitochondrial hyperactivation.iScience · 2025Article
- Review
- Metabolism-driven posttranslational modifications and immune regulation: Emerging targets for immunotherapy.Science advances · 2025Review
- Live fast, die young: neutrophils streamline their metabolism to maximize inflammation.Infection and immunity · 2025Review
- Extracellular ATP regulates phagocytic activity, mitochondrial respiration, and cytokine secretion of human astrocytic cells.Purinergic signalling · 2025Article
- Adenosine accumulation in the blood of newborn mice weakens antimicrobial host defenses.Journal of leukocyte biology · 2025Article
- Metabolic phenotype of bovine blood-derived neutrophils is altered in milk.Scientific reports · 2025Article
- Neutrophil Heterogeneity in Wound Healing.Biomedicines · 2025Review
- Mitochondrial metabolism is rapidly re-activated in mature neutrophils to support stimulation-induced response.bioRxiv : the preprint server for biology · 2025Article
- Article
- Mitochondrial metabolism is rapidly re-activated in mature neutrophils to support stimulation-induced response.Frontiers in immunology · 2025Article
- Dynamic regulation of neutrophil immunometabolism by platelet-derived metabolites.Frontiers in immunology · 2025Review
- Carbohydrate metabolism in supporting and regulating neutrophil effector functions.Current opinion in immunology · 2024Review
- Pharmacological interaction and immune response of purinergic receptors in therapeutic modulation.Purinergic signalling · 2024Review
- Impaired ATP hydrolysis in blood plasma contributes to age-related neutrophil dysfunction.Immunity & ageing : I & A · 2024Article
- Article
- Whole blood RNA sequencing identifies transcriptional differences between primary sclerosing cholangitis and ulcerative colitis.JHEP reports : innovation in hepatology · 2024Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Polymorphonuclear neutrophils (PMNs) form the first line of defense against invading microorganisms. We have shown previously that ATP release and autocrine purinergic signaling via P2Y2 receptors are essential for PMN activation. Here we show that mitochondria provide the ATP that initiates PMN activation. Stimulation of formyl peptide receptors increases the mitochondrial membrane potential (Δψm) and triggers a rapid burst of ATP release from PMNs. This burst of ATP release can be blocked by inhibitors of mitochondrial ATP production and requires an initial formyl peptide receptor-induced Ca(2+) signal that triggers mitochondrial activation. The burst of ATP release generated by the mitochondria fuels a first phase of purinergic signaling that boosts Ca(2+) signaling, amplifies mitochondrial ATP production, and initiates functional PMN responses. Cells then switch to glycolytic ATP production, which fuels a second round of purinergic signaling that sustains Ca(2+) signaling via P2X receptor-mediated Ca(2+) influx and maintains functional PMN responses such as oxidative burst, degranulation, and phagocytosis.
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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.