Evidence map›Paper›PMID 38961399›Full record

ArticleJournal of translational medicine2024

DKK1 loss promotes endometrial fibrosis via autophagy and exosome-mediated macrophage-to-myofibroblast transition.

Zhanqin Zhang, Jianguo Hu

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Methyltransferase-like 3/14-mediated mResearch (Washington, D.C.) · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Mechanistic insights into intrauterine adhesions.Seminars in immunopathology · 2024
    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

2 authors.

Zhanqin ZhangDepartment of Anesthesiology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Jianguo HuDepartment of Obstetrics and Gynecology, Second Affiliated Hospital, Chongqing Medical University, Linjiang Road, No. 76, Chongqing, 400010, China. angeljianguo@163.com.ORCID 0000-0002-7775-6661

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIntrauterine adhesions (IUA) manifest as endometrial fibrosis, often causing infertility or recurrent miscarriage; however, their pathogenesis remains unclear.

objectivesThis study assessed the role of Dickkopf WNT signaling pathway inhibitor 1 (DKK1) and autophagy in endometrial fibrosis, using clinical samples as well as in vitro and in vivo experiments.

methodsImmunohistochemistry, immunofluorescence and western blot were used to determine the localization and expression of DKK1 in endometrium; DKK1 silencing and DKK1 overexpression were used to detect the biological effects of DKK1 silencing or expression in endometrial cells; DKK1 gene knockout mice were used to observe the phenotypes caused by DKK1 gene knockout.

resultsIn patients with IUA, DKK1 and autophagy markers were down-regulated; also, α-SMA and macrophage localization were increased in the endometrium. DKK1 conditional knockout (CKO) mice showed a fibrotic phenotype with decreased autophagy and increased localization of α-SMA and macrophages in the endometrium. In vitro studies showed that DKK1 knockout (KO) suppressed the autophagic flux of endometrial stromal cells. In contrast, ectopic expression of DKK1 showed the opposite phenotype. Mechanistically, we discovered that DKK1 regulates autophagic flux through Wnt/β-catenin and PI3K/AKT/mTOR pathways. Further studies showed that DKK1 KO promoted the secretion of interleukin (IL)-8 in exosomes, thereby promoting macrophage proliferation and metastasis. Also, in DKK1 CKO mice, treatment with autophagy activator rapamycin partially restored the endometrial fibrosis phenotype.

conclusionOur findings indicated that DKK1 was a potential diagnostic marker or therapeutic target for IUA.

Indexed as

AutophagyEndometriumExosomesFibrosisIntercellular Signaling Peptides and ProteinsMacrophagesMice, KnockoutMyofibroblastsAdultAnimalsFemaleHumansMiceMice, Inbred C57BLDKK1 protein, humanDkk1 protein, mouseIntercellular Signaling Peptides and ProteinsDKK1, AutophagyIL-8Intrauterine adhesionsWnt, β-catenin

Identifiers

PMID38961399
PMCPMC11223343

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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 OpenQuestion graph.