Evidence map›Paper›PMID 42078920›Full record

ArticleFrontiers in pharmacology2026

Melatonin: a promising therapy to combat type 2 airway inflammation via MT1-Sirt1 pathway.

Zhe Zhang, Jie Jiang, Guilian Chen, Xiuqin Zhang, Jipeng Wang, Baolan Wang

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Zhe Zhang *Physical Examination Center, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, China.
Jie Jiang *Department of Respiratory Medicine, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, China.
Guilian Chen *Physical Examination Center, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, China.
Xiuqin ZhangDepartment of Respiration Medicine, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Jipeng WangDepartment of Respiratory Medicine, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, China.
Baolan WangDepartment of Respiratory Medicine, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Backgrounds: Type 2 asthma is characterized by airway inflammation, mucus hypersecretion, and remodeling, and circadian rhythm dysregulation is implicated in its pathogenesis. Melatonin, a key circadian hormone, modulates inflammatory signaling, but its role in type 2 airway inflammation remains unclear. This study investigated whether melatonin alleviates airway inflammation and epithelial-mesenchymal transition (EMT) through the melatonin receptor 1 (MT1)-Sirtuin 1 (Sirt1) signaling pathway and circadian clock regulation. Methods: An ovalbumin (OVA)-induced mouse model of type 2 airway inflammation and cultured airway epithelial cells were used. Lung structural remodeling and mucus production were evaluated using hematoxylin and eosin, Masson's trichrome, and periodic acid-Schiff staining. Airway inflammation was assessed by differential inflammatory cell counts in bronchoalveolar lavage fluid. The mRNA and protein expression of circadian clock genes (CRY1 and PER1) and key components of the MT1-Sirt1 pathway were assessed by quantitative real-time PCR, Western blotting, and immunohistochemistry. EMT-related markers were further examined to explore downstream mechanisms. Results: Melatonin treatment activated MT1-Sirt1 signaling and reduced the expression of circadian clock genes CRY1 and PER1. These effects were accompanied by decreased airway inflammation, reduced mucus production, and attenuation of epithelial-mesenchymal transition (EMT) in airway epithelial cells, all of which reached statistical significance. Conclusion: Our findings identify a novel MT1-Sirt1-circadian gene regulatory axis through which melatonin mitigates type 2 airway inflammation and airway remodeling. These results highlight the therapeutic potential of melatonin for type 2 asthma. Limitations include the use of a single animal model and analysis at a single time point.

Indexed as

circadian genesepithelial-mesenchymal transitionmelatoninMT1-Sirt1type 2 airway inflammation

Identifiers

PMID42078920
PMCPMC13133056

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.