ArticleScientific reports2021
Inhibition of the CXCL9-CXCR3 axis suppresses the progression of experimental apical periodontitis by blocking macrophage migration and activation.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 53 citations in OpenAlex.
- Harnessing the structural determinants amenable for polypharmacological behavior of 7D against Sirt1 and CXCR3.iScience · 2026Article
- Macrophage Phenotype Alterations in Treated Periodontitis Patients Suggest a Pro-Inflammatory Bias.Journal of periodontal research · 2026Article
- A CRISPR array orchestrates virulence and host response inMicrobiology spectrum · 2026Article
- CXCR3 is associated with T-cell-induced heart damage in acute rheumatic fever.Nature communications · 2026Article
- The Dual Role of IP-10/CXCL10 in Liver Injury: From Pathogenic Mediator to Clinical Biomarker and Therapeutic Target.Drug design, development and therapy · 2026Review
- Effect of membrane vesicles produced under different pH conditions on the ability ofJournal of bacteriology · 2025Article
- Cytochrome b5 reductase orchestrates IL-1β production in macrophages through FAD.Cell death & disease · 2025Article
- Identifying Potential Targets for the Interception of Inflammatory Bowel Disease: Toward Precision Prevention.Inflammatory bowel diseases · 2025Review
- Single-cell RNA-sequencing of peripheral blood mononuclear cells reveals the transcriptome profile ofFrontiers in cellular and infection microbiology · 2025Article
- Phosphatidylserine-incorporated exosome mimetics encapsulating CXCR3 antagonist alleviate osteoporosis.Advanced functional materials · 2024Article
- Cell of origin alters myeloid-mediated immunosuppression in lung adenocarcinoma.bioRxiv : the preprint server for biology · 2024Article
- Tuberculous pleural effusion-induced Arg-1Respiratory research · 2024Article
- The Role of Macrophage Efferocytosis in the Pathogenesis of Apical Periodontitis.International journal of molecular sciences · 2024Article
- Sulfated CXCR3 Peptide Trap Use as a Promising Therapeutic Approach for Age-Related Macular Degeneration.Biomedicines · 2024Article
- CAR NK92 Cells Targeting BCMA Can Effectively Kill Multiple Myeloma Cells Both In Vitro and In Vivo.Biomedicines · 2024Article
- T Lymphocyte-Macrophage Hybrid Membrane-Coated Biomimetic Nanoparticles Alleviate Myocarditis via Suppressing Pyroptosis by Targeting Gene Silencing.International journal of nanomedicine · 2024Article
- Mural cell-derived chemokines provide a protective niche to safeguard vascular macrophages and limit chronic inflammation.Immunity · 2023Article
- Effect of Lipopolysaccharide-Induced Apical Periodontitis in Diabetes Mellitus Rats on Periapical Inflammation.European journal of dentistry · 2023Article
- Mixed-Culture Propagation of Uterine-Tissue-Resident Macrophages and Their Expression Properties of Steroidogenic Molecules.Biomedicines · 2023Article
- Role ofJournal of oral microbiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apical periodontitis (AP) is an acute or chronic inflammatory disease caused by complex interactions between infected root canal and host immune system. It results in the induction of inflammatory mediators such as chemokines and cytokines leading to periapical tissue destruction. To understand the molecular pathogenesis of AP, we have investigated inflammatory-related genes that regulate AP development. We found here that macrophage-derived CXCL9, which acts through CXCR3, is recruited by progressed AP. The inhibition of CXCL9 by a CXCR3 antagonist reduced the lesion size in a mouse AP model with decreasing IL-1β, IL-6 and TNFα expression. The treatment of peritoneal macrophages with CXCL9 and LPS induced the transmigration and upregulation of osteoclastogenic cytokines such as IL-1β, IL-6 and matrix metalloprotease 2, a marker of activated macrophages. This suggests that the CXCL9-CXCR3 axis plays a crucial role in the development of AP, mediated by the migration and activation of macrophages for periapical tissue destruction. Our data thus show that CXCL9 regulates the functions of macrophages which contribute to AP pathogenesis, and that blocking CXCL9 suppresses AP progression. Knowledge of the principal factors involved in the progression of AP, and the identification of related inflammatory markers, may help to establish new therapeutic strategies.
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.