ArticleCell and tissue research2015
Activation of the NLRP3/caspase-1 inflammasome in human dental pulp tissue and human dental pulp fibroblasts.
Article in Cell and tissue research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.
- Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis-A Systematic Review.Biomolecules · 2022Pooled it
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Let-7a-5p/SHIP-1 Axis Drives SARS-CoV-2 Spike-1-Induced Microglial Pyroptosis.International journal of molecular sciences · 2026Article
- The role of transient receptor potential ankyrin 1 in pyroptosis during pulpitis development.BMC oral health · 2026Article
- Harnessing the Therapeutic Potential of Extracellular Vesicles for Oral Wound Healing.Bioengineering (Basel, Switzerland) · 2026Review
- Emerging Role of the NLRP3 Inflammasome in the Onset of Oral Diseases and Its Potential as a Therapeutic Target.International journal of molecular sciences · 2026Review
- Berberine in oral diseases: molecular mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Decoding signaling crosstalk in pulpitis: pathogenesis and precision therapeutics.Frontiers in cell and developmental biology · 2026Review
- The Role of Inflammasomes in Chronic Oral Inflammatory Disease and Oral Cancer: A Narrative Review.Dentistry journal · 2025Review
- Embracing cancer immunotherapy with manganese particles.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- 3,4-methylenedioxymethamphetamine induces reactive oxygen species-mediated autophagy and thioredoxin-interactive protein/nucleotide-binding domain, leucine-rich containing family, pyrin domain-containing-3 inflammasome activation in dental pulp stem cells.Journal of dental sciences · 2025Article
- Thermosensitive injectable in situ forming hydrogel incorporating anti-oxidative stress and anti-inflammatory nanoparticles for vital pulp therapy of pulpitis.Materials today. Bio · 2025Article
- Roles of Pyroptosis in the Progression of Pulpitis and Apical Periodontitis.Journal of inflammation research · 2025Review
- Pyroptosis in Pulpitis.Journal of inflammation research · 2025Review
- Article
- Guanylate-binding protein 5-mediated autophagy can promote the clearance of intracellular F. nucleatum in dental pulp cells during pulpitis.BMC oral health · 2024Article
- Clustering human dental pulp fibroblasts spontaneously activate NLRP3 and AIM2 inflammasomes and induce IL-1β secretion.Regenerative therapy · 2024Article
- Hypoxia-induced NLRP3 inflammasome activation via the HIF-1α/NF-κB signaling pathway in human dental pulp fibroblasts.BMC oral health · 2024Article
- The protective role of curcumin in human dental pulp stem cells stimulated by lipopolysaccharide via inhibiting NF-κB p65 phosphorylation to suppress NLRP3 inflammasome activation.Clinical oral investigations · 2023Article
- Regulation of caries-induced pulp inflammation by NLRP3 inflammasome: A laboratory-based investigation.International endodontic journal · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
The NLRP3/caspase-1 inflammasome pathway plays an important role in cellular immune defence against bacterial infection; however, its function in human dental pulp tissue and human dental pulp fibroblasts remains poorly understood. We demonstrate that NLRP3 protein expression occurs to a greater extent in pulp tissue with irreversible pulpitis than in normal pulp tissue and in tissue with reversible pulpitis. Caspase-1 is present in its active (cleaved) form only in pulp tissue with irreversible pulpitis. NLRP3 and caspase-1 are expressed in the odontoblast layers in normal human dental pulp tissue, whereas in inflamed pulp tissue, the odontoblast layers are disrupted and dental pulp cells are positive for NLRP3 and caspase-1. Additionally, we investigate the role of the NLRP3/caspase-1 inflammasome pathway in human dental pulp fibroblasts and show that ATP activates the P2X7 receptor on the cell membrane triggering K(+) efflux and inducing the gradual recruitment of the membrane pore pannexin-1. Extracellular lipopolysaccharide is able to penetrate the cytosol and activate NLRP3. Furthermore, the low intracellular K(+) concentration in the cytosol triggers reactive oxygen species generation, which also induces the NLRP3 inflammasome. Thus, the NLRP3/caspase-1 pathway has a biological role in the innate immune response mounted by human dental pulp fibroblasts.
Indexed as
Identifiers
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.