Evidence map›Paper›PMID 30518355›Full record

ArticleRespiratory research2018

Lipoxin A4 receptor agonist BML-111 induces autophagy in alveolar macrophages and protects from acute lung injury by activating MAPK signaling.

Huaizheng Liu, Kefu Zhou, Liangkan Liao, Tianyi Zhang, Mingshi Yang, Chuanzheng Sun

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Respiratory research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Article
  5. Review
  6. MacrophageAutophagy · 2025
    Article
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  8. Transfusion-Related Acute Lung Injury: from Mechanistic Insights to Therapeutic Strategies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  9. Review
  10. Article
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  12. Review
  13. Article
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  15. ERRα protects against sepsis-induced acute lung injury in rats.Molecular medicine (Cambridge, Mass.) · 2023
    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

6 authors at 2 institutions in 1 country.

Huaizheng LiuEmergency and Intensive Care Center, The Third Xiangya Hospital of Central South University, 138 Tongzipo Road, Changsha, 410013, Hunan Province, PR, China.
Kefu ZhouEmergency and Intensive Care Center, The Third Xiangya Hospital of Central South University, 138 Tongzipo Road, Changsha, 410013, Hunan Province, PR, China.
Liangkan LiaoEmergency and Intensive Care Center, The Third Xiangya Hospital of Central South University, 138 Tongzipo Road, Changsha, 410013, Hunan Province, PR, China.
Tianyi ZhangEmergency and Intensive Care Center, The Third Xiangya Hospital of Central South University, 138 Tongzipo Road, Changsha, 410013, Hunan Province, PR, China.
Mingshi YangEmergency and Intensive Care Center, The Third Xiangya Hospital of Central South University, 138 Tongzipo Road, Changsha, 410013, Hunan Province, PR, China.
Chuanzheng SunEmergency and Intensive Care Center, The Third Xiangya Hospital of Central South University, 138 Tongzipo Road, Changsha, 410013, Hunan Province, PR, China. lhz3385@yeah.net.
Third Xiangya Hospital · CNCentral South University · CN

Funding

New Xiangya Talent Project of the Third Xiangya hospital of Central South University No.JY201614
6 · The paper itself

Abstract

backgroundAcute lung injury (ALI) is a life-threatening lung disease where alveolar macrophages (AMs) play a central role both in the early phase to initiate inflammatory responses and in the late phase to promote tissue repair. In this study, we examined whether BML-111, a lipoxin A4 receptor agonist, could alter the phenotypes of AM and thus present prophylactic benefits for ALI.

methodsIn vitro, isolated AMs were treated with lipopolysaccharide (LPS) to induce ALI. In response to BML-111 pre-treatment, apoptosis and autophagy of AMs were examined by flow cytometry, and by measuring biomarkers for each process. The potential involvement of MAPK1 and mTOR signaling pathway was analyzed. In vivo, an LPS-induced septic ALI model was established in rats and the preventative significance of BML-111 was assessed. On the cellular and molecular levels, the pro-inflammatory cytokines TNF-α and IL-6 from bronchoalveolar lavage were measured by ELISA, and the autophagy in AMs examined using Western blot.

resultsBML-111 inhibited apoptosis and induced autophagy of AMs in response to ALI inducer, LPS. The enhancement of autophagy was mediated through the suppression of MAPK1 and MAPK8 signaling, but independent of mTOR signaling. In vivo, BML-111 pre-treatment significantly alleviated LPS-induced ALI, which was associated with the reduction of apoptosis, the dampened production of pro-inflammatory cytokines in the lung tissue, as well as the increase of autophagy of AMs.

conclusionsThis study reveals the prophylactic significance of BML-111 in ALI and the underlying mechanism: by targeting the MAPK signaling but not mTOR pathway, BML-111 stimulates autophagy in AMs, attenuates the LPS-induced cell apoptosis, and promotes the resolution of ALI.

Indexed as

Acute Lung InjuryAnimalsAutophagyEnzyme ActivationHeptanoic AcidsLipopolysaccharidesMacrophages, AlveolarMaleMAP Kinase Signaling SystemRatsRats, Sprague-DawleyReceptors, Lipoxin5(S),6(R)-7-trihydroxyheptanoic acid, methyl esterHeptanoic AcidsLipopolysaccharideslipoxin A(4) receptor, ratReceptors, LipoxinAcute lung injuryApoptosisAutophagyBML-111Lipoxin

Identifiers

PMID30518355
PMCPMC6282312
OpenAlexW2902960319

What OpenQuestion holds

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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.