Evidence map›Paper›PMID 39011034›Full record

ArticleFrontiers in immunology2024

m6A mRNA methylation-mediated MAPK signaling modulates the nasal mucosa inflammatory response in allergic rhinitis.

Ruikun Wang, Jieqiong Liang, Qian Wang, Yiming Zhang, Yingxia Lu, Xiaojun Zhan, Shan Wang, Qinglong Gu

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. [IOX1 alleviates hepatic ischemia-reperfusion injury by inhibiting mitogen-activated protein kinase signaling pathway].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
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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

8 authors.

Ruikun Wang *Department of Otorhinolaryngology Head and Neck Surgery, Children's Hospital, Capital Institute of Pediatrics, Beijing, China.
Jieqiong Liang *Department of Otorhinolaryngology Head and Neck Surgery, Children's Hospital, Capital Institute of Pediatrics, Beijing, China.
Qian WangGraduate School of Peking Union Medical College, Capital Institute of Pediatrics, Beijing, China.
Yiming ZhangDepartment of Otorhinolaryngology Head and Neck Surgery, Children's Hospital, Capital Institute of Pediatrics, Beijing, China.
Yingxia LuDepartment of Otorhinolaryngology Head and Neck Surgery, Children's Hospital, Capital Institute of Pediatrics, Beijing, China.
Xiaojun ZhanDepartment of Otorhinolaryngology Head and Neck Surgery, Children's Hospital, Capital Institute of Pediatrics, Beijing, China.
Shan WangBeijing Municipal Key Laboratory of Child Development and Nutriomics, Capital Institute of Pediatrics, Beijing, China.
Qinglong GuDepartment of Otorhinolaryngology Head and Neck Surgery, Children's Hospital, Capital Institute of Pediatrics, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Allergic rhinitis (AR) is a complex disease in which gene-environment interactions contribute to its pathogenesis. Epigenetic modifications, such as N6-methyladenosine (m6A) modification of mRNA, play important roles in regulating gene expression in multiple physiological and pathological processes. However, the function of m6A modification in AR and the inflammatory response is poorly understood. Methods: We used the ovalbumin (OVA) and aluminum hydroxide to induce an AR mouse model. Nasal symptoms, histopathology, and serum cytokines were examined. We performed combined m6A and RNA sequencing to analyze changes in m6A modification profiles. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and methylated RNA immunoprecipitation sequencing qPCR (MeRIP-qPCR) were used to verify differential methylation of mRNAs and the m6A methylation level. Knockdown or inhibition of Results: We showed that m6A was enriched in a group of genes involved in MAPK signaling pathway. Moreover, we identified a MAPK pathway involving Conclusion: Together, our data show that m6A dysregulation mediated by ALKBH5, is likely to contribute to inflammation of the nasal mucosa via the MAPK signaling pathway, suggesting that ALKBH5 is a potential biomarker for AR treatment.

Indexed as

AdenosineAlkB Homolog 5, RNA DemethylaseDisease Models, AnimalMAP Kinase Signaling SystemNasal MucosaRhinitis, AllergicRNA, MessengerAnimalsCytokinesFemaleInflammationMethylationMiceMice, Inbred BALB CAdenosineALKBH5 protein, mouseAlkB Homolog 5, RNA DemethylaseCytokinesN-methyladenosineRNA, MessengerALKBH5allergic rhinitisinflammationm6AMAPK pathway

Identifiers

PMID39011034
PMCPMC11246857

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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.