Evidence map›Paper›PMID 41423545›Full record

ArticleScientific reports2025

Irisin activates the AMPK-Beclin1 signaling pathway to regulate pulmonary autophagy induced by CSE + LPS.

Zelin Chen, Siyu Wu, Zina Bai, Tongxinwei Sun, Cuiqing Ma, Yahong Chen, Ping Jiang, Aihong Meng

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Observational
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.

Zelin ChenDepartment of Pulmonary and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shi-jiazhuang, 050000, Hebei, People's Republic of China.
Siyu WuDepartment of Pulmonary and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shi-jiazhuang, 050000, Hebei, People's Republic of China.
Zina BaiDepartment of Pulmonary and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shi-jiazhuang, 050000, Hebei, People's Republic of China.
Tongxinwei SunDepartment of Pulmonary and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shi-jiazhuang, 050000, Hebei, People's Republic of China.
Cuiqing MaKey Laboratory of Immune Mechanism and Intervention on Serious Disease in Hebei Province, Shijiazhuang, 050000, Hebei, People's Republic of China.
Yahong ChenDepartment of Pulmonary and Critical Care Medicine, Peking University Third Hospital, 49 Huayuan North Road, Haidian District, Beijing, 100191, China.
Ping JiangDepartment of Pulmonary and Critical Care Medicine, Tianjin First Central Hospital, 24 Fukang road, Nankai District, Tianjin, 300192, China.
Aihong MengDepartment of Pulmonary and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shi-jiazhuang, 050000, Hebei, People's Republic of China. mah123@hebmu.edu.cn.

Funding

Hebei Natural Science Foundation Joint Research Program for Basic Science Cooperation in the Beijing-Tianjin-Hebei Region Grant No.H2023206909/J230030/S23ZX16013Key Project of Precision Medicine Joint Fund of Hebei Province C2021206011
6 · The paper itself

Abstract

Smoking and infection are the most common risk factors for acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Irisin is a hormone-like substance that helps reduce oxidative stress and inflammation in lung diseases. This study aims to explore the potential regulatory mechanism of irisin in AECOPD induced by CSE combined with LPS. Autophagy-deficient models were established in mice and MH-S cells. Pathological changes in mouse lung tissues were assessed using HE staining, while Irisin expression was detected via immunofluorescence. Levels of IL-1β, IL-6, and TNF-α in mouse BALF and MH-S cell supernatants were measured by ELISA. Autophagic flux in MH-S cells was monitored using the Ad-mCherry-GFP-LC3B dual-fluorescence system and transmission electron microscopy. Western blotting was performed to analyze autophagy-related proteins in mice and MH-S cells, elucidating the molecular mechanism of Irisin's protective effects. Irisin can reduce the accumulation of the autophagy marker protein P62 and promote the conversion of LC3-I to LC3-II through the AMPK-Beclin1 pathway, increase autophagosome-lysosome formation, effectively restore damaged autophagic flux, and lower the levels of pro-inflammatory factors IL-1β, IL-6, and TNF-α elevated by CSE + LPS. Irisin activates protective autophagy through the AMPK-Beclin1 pathway, restores the autophagy imbalance induced by CSE + LPS in the lungs, reduces lung inflammation levels, and provides a new therapeutic target for the treatment of AECOPD.

Indexed as

AMP-Activated Protein KinasesAutophagyBeclin-1FibronectinsLipopolysaccharidesLungPulmonary Disease, Chronic ObstructiveSignal TransductionAnimalsMaleMiceMice, Inbred C57BLAMP-Activated Protein KinasesBeclin-1Becn1 protein, mouseFibronectinsFNDC5 protein, mouseLipopolysaccharidesCigaretteInflammationIrisinSmoke

Identifiers

PMID41423545
PMCPMC12722212

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.