Evidence map›Paper›PMID 35742971›Full record

ArticleInternational journal of molecular sciences2022

Selective Elimination of Senescent Fibroblasts by Targeting the Cell Surface Protein ACKR3.

Kento Takaya, Toru Asou, Kazuo Kishi

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. 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

3 authors at 1 institution in 1 country.

Kento TakayaDepartment of Plastic and Reconstructive Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.ORCID 0000-0001-8992-2762
Toru AsouDepartment of Plastic and Reconstructive Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Kazuo KishiDepartment of Plastic and Reconstructive Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Keio University · JP

Funding

Japan Society for the Promotion of Science JP 20K18422
6 · The paper itself

Abstract

The accumulation of senescent cells in aging tissues is associated with age-related diseases and functional decline. Thus, senolysis, a therapy aimed at rejuvenation by removing senescent cells from the body, is being developed. However, this therapy requires the identification of membrane surface antigens that are specifically expressed on senescent cells for their selective elimination. We showed that atypical chemokine receptor 3 (ACKR3), a receptor of the CXC motif chemokine 12 (CXCL12) implicated in cancer, inflammation, and cardiovascular disorders, is selectively expressed on the surface of senescent human fibroblasts but not on proliferating cells. Importantly, the differential presence of ACKR3 enabled the isolation of senescent cells by flow cytometry using anti-ACKR3 antibodies. Furthermore, antibody-dependent cellular cytotoxicity assays revealed that cell surface ACKR3 preferentially sensitizes senescent but not dividing fibroblasts to cell injury by natural killer cells. Conclusively, the selective expression of ACKR3 on the surface of senescent cells allows the preferential elimination of senescent cells. These results might contribute to the future development of novel senolysis approaches.

Indexed as

Membrane ProteinsCellular SenescenceChemokine CXCL12FibroblastsFlow CytometryHumansKiller Cells, NaturalReceptors, CXCRACKR3 protein, humanChemokine CXCL12Membrane ProteinsReceptors, CXCRantibody-dependent cellular cytotoxicityatypical chemokine receptor 3fibroblastnatural killer cellsenolysis

Identifiers

PMID35742971
PMCPMC9223754
OpenAlexW4281765859

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.