Evidence map›Paper›PMID 33313951›Full record

ArticleMolecular medicine reports2021

circARRDC3 contributes to interleukin‑13‑induced inflammatory cytokine and mucus production in nasal epithelial cells via the miR‑375/KLF4 axis.

Tao Wang, Peihua Wang, Dong Chen, Zhou Xu, Liyun Yang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Research progress on circRNAs in type 2 CRS.Frontiers in immunology · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Circular RNAs: emerging players in asthma and COPD.Frontiers in cell and developmental biology · 2023
    Review
  10. Recent miRNA Research in Asthma.Current allergy and asthma reports · 2022
    Review
  11. Review
  12. Review
  13. Review
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Tao WangDepartment of Otolaryngology Head and Neck Surgery, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200011, P.R. China.
Peihua WangDepartment of Otolaryngology Head and Neck Surgery, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200011, P.R. China.
Dong ChenDepartment of Otolaryngology Head and Neck Surgery, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200011, P.R. China.
Zhou XuDepartment of Otolaryngology Head and Neck Surgery, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200011, P.R. China.
Liyun YangDepartment of Otolaryngology Head and Neck Surgery, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200011, P.R. China.
Shanghai Jiao Tong University · CNShanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allergic rhinitis (AR) is a common inflammatory disorder of the nasal mucosa. It is a major risk factor for asthma development, and uncontrolled AR can lead to the worsening of asthma symptoms, which affects the quality of life and productivity of patients. Circular RNAs (circRNA) were reported to be involved in the pathogenesis of AR. The aim of the present study was to investigate the functional role of circRNA arrestin domain‑containing 3 (circARRDC3) in AR progression. circARRDC3 knockdown suppressed the levels of granulocyte‑macrophage colony‑stimulating factor (GM‑CSF) and eotaxin and mucin 5AC (MUC5AC) in IL‑13‑induced nasal epithelial cells. Moreover, circARRDC3 silencing promoted viability and suppressed apoptosis in IL‑13‑induced NECs. circARRDC3 targeted microRNA (miR)‑375 and negatively regulated its expression. miR‑375 inhibition reversed the effects of circARRDC3 knockdown on GM‑CSF, eotaxin and MUC5AC expression levels, cell viability and cell apoptosis. In addition, miR‑375 inhibited krueppel‑like factor 4 (KLF4) expression through direct interaction, and miR‑375 overexpression inhibited GM‑CSF, eotaxin and MUC5AC expression levels, and cell apoptosis, which was abolished following KLF4 overexpression. In addition, circARRDC3, miR‑375 and KLF4 were all dysregulated in the nasal mucosa of patients with AR. miR‑375 expression was negatively correlated with circARRDC3 and KLF4 expression, and circARRDC3 expression was positively correlated with KLF4 expression. In conclusion, circARRDC3 contributed to the development of AR by regulating the miR‑375/KLF4 axis. These findings may provide novel insights into the pathogenesis of AR.

Indexed as

AdolescentAdultApoptosisArrestinsCells, CulturedCell SurvivalChemokine CCL11CytokinesEpithelial CellsFemaleGranulocyte-Macrophage Colony-Stimulating FactorHumansInflammationInterleukin-13Kruppel-Like Factor 4Kruppel-Like Transcription FactorsARRDC3 protein, humanArrestinsCCL11 protein, humanChemokine CCL11CytokinesGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-13KLF4 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsMicroRNAsMIRN375 microRNA, humanMucin 5ACRNA, Circularallergic rhinitiscircular RNA arrestin domain‑containing 3Krueppel‑like factor 4microRNA‑375

Identifiers

PMID33313951
PMCPMC7751456
OpenAlexW3112813018

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.