Evidence map›Paper›PMID 24923883›Full record

ArticleBritish journal of pharmacology2014

Lipoxin A4 suppresses the development of endometriosis in an ALX receptor-dependent manner via the p38 MAPK pathway.

Rongfeng Wu, Weidong Zhou, Shuo Chen, Yan Shi, Lin Su, Maobi Zhu, Qionghua Chen, Qingxi Chen

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.4field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 52 citations in OpenAlex.

  1. Trial
  2. Anti-Inflammatory Effects of Lipoxin A4 inAnimals : an open access journal from MDPI · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
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  12. Article
  13. Review
  14. 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

8 authors at 2 institutions in 1 country.

Rongfeng WuState Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China.
Weidong Zhou
Shuo Chen
Yan Shi
Lin Su
Maobi Zhu
Qionghua Chen
Qingxi Chen
First Affiliated Hospital of Xiamen University · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeLipoxins can function as endogenous 'breaking signals' in inflammation and play important roles in the progression of endometriosis. In this study, we further investigated the molecular mechanism by which lipoxin A4 (LXA4 ) suppresses the development of endometriosis. EXPERIMENTAL APPROACH: Primary endometriotic stromal cells (ESCs) were treated with IL-1β, or pre-incubated with LXA4 before incubation with IL-1β. The LXA4 receptor (ALX receptor) antagonist Boc-2 and gene-silencing approaches were used to study the involvement of the ALX receptor in anti-inflammatory signalling responses in ESCs. An animal model of endometriosis was induced in BALB/c mice by i.p. injection of an endometrium-rich fragment. KEY

resultsDecreased levels of LXA4 and 15-LOX-2 expression but increased expression of AXL receptors were observed in endometriotic tissues. LXA4 inhibited the release of inflammatory factors and phosphorylation of p38 MAPK in IL-1β-induced ESCs, an effect mediated by ALX receptors. LXA4 inhibited the proliferation of ESCs, as indicated by reduced DNA replication, caused G0 /G1 phase cell cycle arrest and down-regulated the expression of proliferating cell nuclear antigen in ESCs. LXA4 also attenuated the invasive activity of ESCs mainly by suppressing the expression and activity of MMP-9. In vivo, we further confirmed that LXA4 could inhibit the progression of endometriosis by acting as an anti-inflammatory. CONCLUSIONS AND IMPLICATIONS: LXA4 exerted anti-inflammatory, anti-proliferative and anti-invasive effects on endometriosis through a mechanism that involved down-regulating the activities of p38 MAPK, which was mediated by ALX receptors.

Indexed as

AnimalsArachidonate 15-LipoxygenaseCells, CulturedCytokinesEndometriosisEndometriumFemaleGene SilencingHumansLipoxinsMatrix Metalloproteinase 9Mice, Inbred BALB Cp38 Mitogen-Activated Protein KinasesReceptors, LipoxinStromal CellsALOX15B protein, humanArachidonate 15-LipoxygenaseCytokineslipoxin A4LipoxinsMatrix Metalloproteinase 9p38 Mitogen-Activated Protein KinasesReceptors, Lipoxin

Identifiers

PMID24923883
PMCPMC4294115
OpenAlexW1507060320

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.