Evidence map›Paper›PMID 32959976›Full record

ArticleAging cell2020

CXCL5-CXCR2 signaling is a senescence-associated secretory phenotype in preimplantation embryos.

Yuta Kawagoe, Ikko Kawashima, Yorino Sato, Naoki Okamoto, Kazuei Matsubara, Kazuhiro Kawamura

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Senolytic Therapy as a Preventive Strategy for Spine Degeneration and Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Review
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  9. Magnolin Mitigates Skin Ageing Through the CXCL10/p38 Signalling Pathway.Journal of cellular and molecular medicine · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Review
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  15. Article
  16. Article
  17. Science advances · 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 3 institutions in 1 country.

Yuta KawagoeDepartment of Obstetrics and Gynecology, Advanced Reproduction Research Center, International University of Health and Welfare School of Medicine, Narita, Japan.ORCID 0000-0002-0641-1244
Ikko KawashimaInstitute of Advanced BioMedical Engineering and Science, Tokyo Women's Medical University, Shinjuku-ku, Japan.
Yorino SatoDepartment of Obstetrics and Gynecology, Advanced Reproduction Research Center, International University of Health and Welfare School of Medicine, Narita, Japan.
Naoki OkamotoDepartment of Obstetrics and Gynecology, Advanced Reproduction Research Center, International University of Health and Welfare School of Medicine, Narita, Japan.
Kazuei MatsubaraThe United Graduate School of Agriculture Sciences, Iwate University, Morioka, Japan.
Kazuhiro KawamuraDepartment of Obstetrics and Gynecology, Advanced Reproduction Research Center, International University of Health and Welfare School of Medicine, Narita, Japan.
International University of Health and Welfare · JPIwate University · JPTokyo Women's Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pregnancy rate of women decreases with age due to declining quality of oocytes and embryos. However, there is no established method to improve pregnancy rate in aging women. In this study, we identified a senescence-associated secretory phenotype (SASP) factor partially responsible for the decline in embryo implantation potential. Based on microarray analysis using young and aging human embryos at the same morphological grade, 702 genes showed >fivefold increases in aging human blastocysts. Among these genes, C-X-C motif chemokine 5 (CXCL5) showed 7.7-fold increases in aging human blastocysts. However, no-age-dependent changes in expression of the CXCR2, the cognate receptor for CXCL5, were found. In aging mice, Cxcl5 transcript levels were also increased in oocytes and embryos. Treatment of young mouse embryos with CXCL5 decreased implantation rates, together with increased expression of aging markers (P53, P21, Pai-1, and Il-6). Moreover, CXCL5 treatment suppressed trophoblast outgrowth in young mouse blastocysts. Conversely, suppression of CXCL5-CXCR2 signaling in aging mouse embryos using neutralizing antibodies and a receptor antagonist improved the implantation rate, leading to increases in pregnancy and delivery of normal pups. The gene expression pattern of these embryos was comparable to that in young mouse embryos showing enriched cell proliferation-related pathways. In conclusion, we identified CXCL5 as a SASP factor in human and mouse embryos and suppression of CXCL5-CXCR2 signaling during embryo culture improved pregnancy success in aging mice. Future analysis on CXCL5-CXCR2 signaling suppression in human embryos could be the basis to improve embryo development and pregnancy outcome in middle-aged infertile patients.

Indexed as

AdultAnimalsBlastocystCellular SenescenceChemokine CXCL5FemaleHumansMaleMiceMice, Inbred ICRMiddle AgedReceptors, Interleukin-8BSignal TransductionChemokine CXCL5CXCL5 protein, humanCxcl5 protein, mouseCXCR2 protein, humanCxcr2 protein, mouseReceptors, Interleukin-8BagingCXCL5CXCR2infertilitypreimplantation embryoSASP

Identifiers

PMID32959976
PMCPMC7576282
OpenAlexW3087321107

What OpenQuestion holds

Textmetadata
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.