Evidence map›Paper›PMID 35922870›Full record

ArticleStem cell research & therapy2022

Overexpressing HPGDS in adipose-derived mesenchymal stem cells reduces inflammatory state and improves wound healing in type 2 diabetic mice.

Long Ouyang, Daojing Qiu, Xin Fu, Aiping Wu, Pengyuan Yang, Zhigang Yang, Qian Wang, Li Yan, Ran Xiao

Open access · goldAbstract read
In one paragraph

Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.3field-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

27 citing papers in PubMed, 35 citations in OpenAlex.

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  13. [Molecular mechanism of high-altitude hypoxia-induced lipid metabolism disorder in mouse spleen tissue].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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  17. Proteomic Associations of Adverse Outcomes in Human Heart Failure.Journal of the American Heart Association · 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 3 institutions in 1 country.

Long Ouyang *Research Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China.ORCID 0000-0002-2116-320X
Daojing Qiu *Research Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China.
Xin FuResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China.
Aiping WuSuzhou Institute of Systems Medicine, Suzhou, Jiangsu, People's Republic of China.
Pengyuan YangKey Laboratory of Infection and Immunity of CAS, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, People's Republic of China.
Zhigang YangResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China.
Qian WangResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China.
Li YanResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China.
Ran XiaoResearch Center of Plastic Surgery Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, People's Republic of China. xiaoran@psh.pumc.edu.cn.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNChinese Academy of Sciences · CNSuzhou Institute of Systems Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn diabetes, delayed wound healing was considered as the result of excessive recruitment and retention of pro-inflammatory cells and factors. Hematopoietic prostaglandin D synthase (HPGDS) was identified from differently expressed genes of diabetic human foot skin. HPGDS is responsible for the production of prostaglandin D2 (PGD2), an inflammatory mediator. Therefore, we aim to explore whether HPGDS could be a therapeutic target in the diabetic wound (DW).

methodIn this study, we compared gene expression profilings of diabetic human foot skin and non-diabetic human foot skin from the Gene Expression Omnibus database. We detected the characteristics of immune components in diabetic mice wound and investigated the role and underlying mechanism of the differently expressed Hpgds for the diabetic wound healing. For in vivo studies, we engineered ADSC to overexpress Hpgds (ADSC

resultsHpgds was significantly down-regulated in type 2 diabetic mice wound and its deficiency delayed normal wound healing. ADSC

conclusionOur results demonstrated that Hpgds is required for wound healing, and ADSC

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Mesenchymal Stem CellsAnimalsCulture Media, ConditionedHumansIntramolecular OxidoreductasesMiceProstaglandin D2Stem CellsWound HealingCulture Media, ConditionedHPGDS protein, mouseIntramolecular OxidoreductasesProstaglandin D2ADSCDiabetic woundHealingHpgdsInflammation regulator

Identifiers

PMID35922870
PMCPMC9351105
OpenAlexW4289711193

What OpenQuestion holds

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LicenceCC BY
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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.