Evidence map›Paper›PMID 34887659›Full record

ArticleInternational journal of nanomedicine2021

Extracellular Vesicles from HIF-1α-Overexpressing Adipose-Derived Stem Cells Restore Diabetic Wounds Through Accelerated Fibroblast Proliferation and Migration.

Jie Wang, Hao Wu, Yue Zhao, Youyou Qin, Yingbo Zhang, Hao Pang, Yongting Zhou, Xueyi Liu, Zhibo Xiao

Open access · goldAbstract read
In one paragraph

Article in International journal of nanomedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
2.8field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

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  9. Advances in the Role of Stem Cell-Derived Exosomes in Diabetic Foot Wound Healing.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025
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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.

Jie Wang *Department of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Hao Wu *Department of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Yue ZhaoDepartment of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Youyou QinDepartment of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Yingbo ZhangDepartment of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Hao PangDepartment of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Yongting ZhouDepartment of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Xueyi LiuDepartment of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Zhibo XiaoDepartment of Plastic and Aesthetic Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, People's Republic of China.
Harbin Medical University · CNSecond Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeInhibition of cellular adaptation to hypoxia can cause persistent inflammation, thereby increasing tissue damage and complicating wound healing in diabetes patients. Regulating cellular adaptation to hypoxic environments can help in effective wound repair. Hypoxia-inducible factor (HIF)-1 MATERIALS AND

methodsHIF-1α expression in diabetes patients and healthy participants was studied. High-throughput sequencing, GO, and KEGG analysis revealed that ADSCs small extracellular vesicle hypoxia environments may increase HIF-1α expression by affecting cell metabolism, differentiation, and TGF-β secretion, or by altering the PI3K/AKT pathway. Effect of addition of ADSCs-hEVs on cell proliferation and migration was investigated using Western blotting, EdU assay, transwell assay, and migration. In vivo, after 7, 14, and 21 days, important factors for diabetic wound healing were evaluated by immunohistochemistry, qRT-PCR, Masson staining, and H&E staining.

resultsHIF-1α expression decreased in the skin of diabetes patients; interleukin (IL)-6 expression increased, and growth factor-related indexes decreased. ADSCs-hEVs significantly increased the expression and secretion of growth factors, compared with ADSCs-EVs. In vivo, ADSC-hEV treatment accelerated the healing rate and improved the healing quality of diabetic wounds compared with ADSCs-EVs.

conclusionSpeed and quality of wound healing increased significantly in the ADSCs-hEVs group, which could inhibit early inflammation while promoting the secretion and expression of growth factors and extracellular matrix-related indexes.

Indexed as

Diabetes MellitusExtracellular VesiclesCell ProliferationFibroblastsHumansHypoxia-Inducible Factor 1, alpha SubunitPhosphatidylinositol 3-KinasesStem CellsWound HealingHypoxia-Inducible Factor 1, alpha SubunitPhosphatidylinositol 3-KinasesADSCsdiabetic woundextracellular vesiclesfibroblastHIF-1α

Identifiers

PMID34887659
PMCPMC8652947
OpenAlexW4200466502

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.