Mechanistic studies on the role of CHI3L1 in eosinophilic inflammation in chronic sinusitis.

Ling Guo, Yi Peng, Cheng Yang, Xinghong Liu, Weilan Xiong, Weijiang Liao, Jiangang Fan

Abstract readReview

In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing 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

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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

1 citing paper in PubMed.

Characteristics ofFrontiers in immunology · 2025
Article

4 · The record

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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

7 authors.

Ling GuoDepartment of Otolaryngology Head and Neck Surgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.

Yi PengDepartment of Otolaryngology Head and Neck Surgery, Chengdu Second People's Hospital, Chengdu, China.

Cheng YangDepartment of Otolaryngology Head and Neck Surgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.

Xinghong LiuDepartment of Otolaryngology Head and Neck Surgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.

Weilan XiongDepartment of Otolaryngology Head and Neck Surgery, Sichuan Provincial People's Hospital, Chengdu University of Traditional Chinese Medicine, Chengdu, China.

Weijiang LiaoDepartment of Otolaryngology Head and Neck Surgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.

Jiangang FanDepartment of Otolaryngology Head and Neck Surgery, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

More than 10% of adults suffer from chronic rhinosinusitis (CRS), a chronic inflammatory condition that lowers quality of life, reduces productivity, and shortens work hours. Every year, more than 1 million surgeries are performed worldwide as a result of CRS. In recent years, targeted therapy for CRS has become a hotspot of research at home and abroad and has made significant progress, but CRS still has a high recurrence rate. Therefore CRS urgently needs precise targeted therapy. In the pathological process of CRS, the involvement of eosinophils is an important inflammatory mechanism. And excessive aggregation of eosinophils often leads to severe inflammatory responses. Studies have shown that chitinase 3-like protein 1 (CHI3L1) plays a key role in the activation and migration of eosinophils. This review will combine the latest research results to analyse in detail the biological properties of CHI3L1, its expression pattern in CRS, and the possible mechanisms by which it affects eosinophil aggregation by regulating immune responses and inflammatory processes, which will provide insights into the key role of CHI3L1 in the pathological process of CRS and offer a new target for the treatment of CRS.

Indexed as

Chitinase-3-Like Protein 1EosinophilsInflammationRhinitisSinusitisAnimalsChronic DiseaseHumansCHI3L1 protein, humanChitinase-3-Like Protein 1CHI3L1chronic sinusitiseosinophilsimmunomodulationinflammatory mechanisms

Identifiers

PMID40201175

DOI10.3389/fimmu.2025.1562546

PMCPMC11975569

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