Evidence map›Paper›PMID 34181194›Full record

ArticleFrontiers of medicine2021

Particulate matter 2.5 triggers airway inflammation and bronchial hyperresponsiveness in mice by activating the SIRT2-p65 pathway.

Manling Liu, Zhaoling Shi, Yue Yin, Yishi Wang, Nan Mu, Chen Li, Heng Ma, Qiong Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Frontiers of medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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  7. Review
  8. Preventive nutrition and food science · 2022
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  9. Article
  10. Review
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 at 2 institutions in 1 country.

Manling Liu *Department of Physiology and Pathophysiology, Fourth Military Medical University, Xi'an, 710032, China.
Zhaoling Shi *Department of Pediatrics, Second Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, 712046, China.
Yue Yin *Department of Physiology and Pathophysiology, Fourth Military Medical University, Xi'an, 710032, China.
Yishi WangDepartment of Physiology and Pathophysiology, Fourth Military Medical University, Xi'an, 710032, China.
Nan MuDepartment of Physiology and Pathophysiology, Fourth Military Medical University, Xi'an, 710032, China.
Chen LiDepartment of Physiology and Pathophysiology, Fourth Military Medical University, Xi'an, 710032, China. shaoyuan@fmmu.edu.cn.
Heng MaDepartment of Physiology and Pathophysiology, Fourth Military Medical University, Xi'an, 710032, China. hengma@fmmu.edu.cn.
Qiong WangDepartment of Cardiovascular Medicine, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China. wangqiong@fmmu.edu.cn.
Air Force Medical University · CNAffiliated Hospital of Shaanxi University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to particulate matter 2.5 (PM2.5) potentially triggers airway inflammation by activating nuclear factor-κB (NF-κB). Sirtuin 2 (SIRT2) is a key modulator in inflammation. However, the function and specific mechanisms of SIRT2 in PM2.5-induced airway inflammation are largely understudied. Therefore, this work investigated the mechanisms of SIRT2 in regulating the phosphorylation and acetylation of p65 influenced by PM2.5-induced airway inflammation and bronchial hyperresponsiveness. Results revealed that PM2.5 exposure lowered the expression and activity of SIRT2 in bronchial tissues. Subsequently, SIRT2 impairment promoted the phosphorylation and acetylation of p65 and activated the NF-κB signaling pathway. The activation of p65 triggered airway inflammation, increment of mucus secretion by goblet cells, and acceleration of tracheal stenosis. Meanwhile, p65 phosphorylation and acetylation, airway inflammation, and bronchial hyperresponsiveness were deteriorated in SIRT2 knockout mice exposed to PM2.5. Triptolide (a specific p65 inhibitor) reversed p65 activation and ameliorated PM2.5-induced airway inflammation and bronchial hyperresponsiveness. Our findings provide novel insights into the molecular mechanisms underlying the toxicity of PM2.5 exposure. Triptolide inhibition of p65 phosphorylation and acetylation could be an effective therapeutic approach in averting PM2.5-induced airway inflammation and bronchial hyperresponsiveness.

Indexed as

Particulate MatterSignal TransductionSirtuin 2AnimalsInflammationMiceNF-kappa BTranscription Factor RelANF-kappa BParticulate MatterRela protein, mouseSirt2 protein, mouseSirtuin 2Transcription Factor RelAairway inflammationbronchial hyperresponsivenessp65particulate matter 2.5sirtuin 2triptolide

Identifiers

PMID34181194
OpenAlexW3175563416

What OpenQuestion holds

Textmetadata
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.