Evidence map›Paper›PMID 35383267›Full record

ArticleCommunications biology2022

Altered regulation of mesenchymal cell senescence in adipose tissue promotes pathological changes associated with diabetic wound healing.

Arisa Kita, Yuki Saito, Norihiro Miura, Maki Miyajima, Sena Yamamoto, Tsukasa Sato, Takatoshi Yotsuyanagi, Mineko Fujimiya, Takako S Chikenji

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

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  9. Evolution of the Cdk4/6-Cdkn2 system in invertebrates.Genes to cells : devoted to molecular & cellular mechanisms · 2024
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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

9 authors at 2 institutions in 1 country.

Arisa KitaDepartment of Plastic and Reconstructive Surgery, Sapporo Medical University, Sapporo, Japan.ORCID http://orcid.org/0000-0001-5130-6075
Yuki SaitoDepartment of Anatomy, Sapporo Medical University School of Medicine, Sapporo, Japan. yuki.saito@sapmed.ac.jp.ORCID http://orcid.org/0000-0002-7949-1628
Norihiro MiuraGraduate School of Health Sciences, Hokkaido University, Sapporo, Japan.
Maki MiyajimaGraduate School of Health Sciences, Hokkaido University, Sapporo, Japan.
Sena YamamotoGraduate School of Health Sciences, Hokkaido University, Sapporo, Japan.
Tsukasa SatoGraduate School of Health Sciences, Hokkaido University, Sapporo, Japan.
Takatoshi YotsuyanagiDepartment of Plastic and Reconstructive Surgery, Sapporo Medical University, Sapporo, Japan.
Mineko FujimiyaDepartment of Anatomy, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takako S ChikenjiDepartment of Anatomy, Sapporo Medical University School of Medicine, Sapporo, Japan. chikenji@pop.med.hokudai.ac.jp.ORCID http://orcid.org/0000-0003-2832-3656
Sapporo Medical University · JPSapporo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pathologic diabetic wound healing is caused by sequential and progressive deterioration of hemostasis, inflammation, proliferation, and resolution/remodeling. Cellular senescence promotes wound healing; however, diabetic wounds exhibit low levels of senescent factors and accumulate senescent cells, which impair the healing process. Here we show that the number of p15

Indexed as

Diabetes Mellitus, ExperimentalMesenchymal Stem CellsAdipose TissueAnimalsCellular SenescenceMiceWound Healing

Identifiers

PMID35383267
PMCPMC8983691
OpenAlexW4224312638

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.