Evidence map›Paper›PMID 33782389›Full record

ArticleCell death discovery2021

Vagus nerve stimulation enhances the cholinergic anti-inflammatory pathway to reduce lung injury in acute respiratory distress syndrome via STAT3.

Sheng Li, Di Qi, Jia-Ni Li, Xin-Yu Deng, Dao-Xin Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Vagus nerve stimulation and pulmonary outcomes: a scoping review of preclinical and clinical evidence.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026
    Article
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  8. Review
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  12. Article
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  15. Rewiring the Lung-CNS Axis After Spinal Cord Injury.Journal of inflammation research · 2026
    Review
  16. Review
  17. Article
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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

5 authors at 3 institutions in 1 country.

Sheng LiDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Chongqing Medical University, 400010, Chongqing, China.
Di QiDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Chongqing Medical University, 400010, Chongqing, China.
Jia-Ni LiDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, 400010, Chongqing, China.
Xin-Yu DengDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Chongqing Medical University, 400010, Chongqing, China. sinvee@126.com.
Dao-Xin WangDepartment of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Chongqing Medical University, 400010, Chongqing, China. wangdaoxin1@163.com.
Chongqing Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CNDalian Medical University · CN

Funding

Natural Science Foundation of Chongqing (Natural Science Foundation of Chongqing Municipality) cstc2019jcyj-zdxmX0031
6 · The paper itself

Abstract

The cholinergic anti-inflammatory pathway (CAIP) is important for antagonizing inflammation and treating several diseases, including acute respiratory distress syndrome (ARDS), and is related to vagus nerve integrity. However, its underlying pathophysiological mechanism is still unclear. We hypothesized that CAIP regulates lung injury repair after ARDS through the STAT3 signaling pathway, which is an important downstream effector of α7nAchR. We enhanced CAIP activity by subjecting rats to vagus nerve stimulation (VNS), and administered the α-7 acetylcholine receptor (α7nAchR) agonist and antagonist to determine whether VNS can reduce lung injury by regulating the pulmonary inflammatory response through CAIP. After being subjected to VNS, the secretion of TNF-α and IL-1β was decreased, while the level of IL-10 was increased in the rat model of ARDS. Moreover, VNS treatment reduced lung mRNA levels of M1 macrophage markers, while increased those of M2 macrophage markers. The expression of Caspase-1 decreased, while that of STAT3 increased in lung tissue after VNS treatment. The aforementioned effects of VNS were reversed by cutting the cervical vagus efferent branch and blocking α7nAchR. These findings suggest that VNS inhibits the ARDS inflammatory response by promoting CAIP activity. Next, we used lentivirus knockdown of STAT3 expression to explore the mechanism of VNS through CAIP on lung inflammation in ARDS model rats. VNS activates α7nAchR, increases STAT3 expression, reduces Caspase-1 expression, suppresses inflammation by inhibiting inflammatory pyroptosis and M1 to M2 macrophage transformation, which may constitute the main mechanism of VNS action in ARDS.

Identifiers

PMID33782389
PMCPMC8005666
OpenAlexW3140424755

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.