ArticleClinical and translational allergy2018
The kinase LRRK2 is differently expressed in chronic rhinosinusitis with and without nasal polyps.
Article in Clinical and translational allergy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 11 citations in OpenAlex.
- IRF4 Knockdown Inhibits the Chronic Rhinosinusitis Without Nasal Polyps Development by Regulating NLRP3/Caspase-1/GSDMD-Mediated Pyroptosis.Biochemical genetics · 2025Article
- EGF Protects Epithelial Cells from Barrier Damage in Chronic Rhinosinusitis with Nasal Polyps.Journal of inflammation research · 2022Article
- Identification of lncRNA Biomarkers and LINC01198 Promotes Progression of Chronic Rhinosinusitis with Nasal Polyps through Sponge miR-6776-5p.BioMed research international · 2022Article
- Oral P. gingivalis impairs gut permeability and mediates immune responses associated with neurodegeneration in LRRK2 R1441G mice.Journal of neuroinflammation · 2020Article
- Hub Genes Identification in a Murine Model of Allergic Rhinitis Based on Bioinformatics Analysis.Frontiers in genetics · 2020Article
- LRRK2 Biology from structure to dysfunction: research progresses, but the themes remain the same.Molecular neurodegeneration · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic rhinosinusitis (CRS), commonly divided into CRS with nasal polyps (CRSwNP) and without nasal polyps (CRSsNP) is an inflammatory disease which mechanism remain unclear. Leucine-rich repeat kinase 2 (LRRK2) has been proved to be a negative regulator of inflammation response while its role in pathogenesis of CRS has yet to be revealed. This research study was designed to investigate the relationship between the expression level and biologic role of LRRK2 in CRS.
methodsExpression of LRRK2 mRNA and noncoding repressor of NFAT (NRON) were examined by qRT-PCR. Protein levels of LRRK2 were performed by western blot and immunohistochemistry. Nuclear factor of activated T cells (NFAT) nuclear translocation was analyzed by immunohistochemistry. Additionally, LRRK2 mRNA and NRON expression in response to specific inflammatory stimulation was measured in human nasal epithelia cells (HNECs).
resultsThe expression of LRRK2 was increased in CRSsNP patients (
conclusionLRRK2 and NRON may play different role in CRSsNP and CRSwNP. The molecular mechanisms identified here may aid in the design of novel therapeutic strategies to improve clinical outcomes.
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.