Evidence map›Paper›PMID 32787917›Full record

ArticleStem cell research & therapy2020

Exosomes derived from atorvastatin-pretreated MSC accelerate diabetic wound repair by enhancing angiogenesis via AKT/eNOS pathway.

Muyu Yu, Wei Liu, Junxian Li, Junxi Lu, Huijuan Lu, Weiping Jia, Fang Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 244 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
244citing papers in PubMed, 4 pooled it
16.0field-weighted citation impact, top 1% 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

244 citing papers in PubMed, 4 syntheses or guidelines pooled it, 371 citations in OpenAlex.

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  8. Biology and Therapeutic Potential of Exosomes, Targeted Drug Delivery.International journal of molecular sciences · 2026
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184 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 1 country.

Muyu YuDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Wei LiuSpine Center, Department of Orthopaedics, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, 200003, China.
Junxian LiDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Junxi LuDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Huijuan LuDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Weiping JiaDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China.
Fang LiuDepartment of Endocrinology and Metabolism, Shanghai Diabetes Institute, Shanghai Key Laboratory of Diabetes Mellitus, Shanghai Clinical Center for Diabetes, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, 200233, China. f-liu@sjtu.edu.cn.
Shanghai Jiao Tong University · CNShanghai Sixth People's Hospital · CNSecond Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMesenchymal stem cell (MSC)-derived exosomes emerge as promising candidates for treating delayed wound healing in diabetes due to the promotion of angiogenesis. Preconditioned MSC with chemical or biological factors could possibly enhance the biological activities of MSC-derived exosomes. The purpose of this research focused on whether exosomes derived from the bone marrow MSC (BMSC) pretreated with atorvastatin (ATV), could exhibit better pro-angiogenic ability in diabetic wound healing or not and its underlying molecular mechanism.

methodsWe isolated exosomes from non-pretreated BMSC (Exos) and ATV pretreated BMSC (ATV-Exos) and evaluated their characterization by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA) and Western blotting. In vivo, we made full-thickness skin defects in streptozotocin (STZ)-induced diabetic rats and the defects received multiple-point injection with PBS, Exos, or ATV-Exos. Two weeks later, histological analysis was conducted to evaluate the impact of different treatments on wound healing and the neovascularization was measured by micro-CT. In vitro, cell proliferation, migration, tube formation, and vascular endothelial growth factor (VEGF) secretion were measured in human umbilical vein endothelial cells (HUVEC). The role of miRNAs and AKT/eNOS signaling pathway in the promoted angiogenesis of ATV-Exos were assessed with their inhibitors.

resultsNo significant difference in morphology, structure, and concentration was observed between ATV-Exos and Exos. In STZ-induced diabetic rats, ATV-Exos exhibited excellent abilities in facilitating the wound regeneration by promoting the formation of blood vessels compared with Exos without influencing liver and kidney function. Meanwhile, ATV-Exos promoted the proliferation, migration, tube formation, and VEGF level of endothelial cells in vitro. And AKT/eNOS pathway was activated by ATV-Exos and the pro-angiogenic effects of ATV-Exo were attenuated after the pathway being blocked. MiR-221-3p was upregulated by ATV-Exos stimulation, and miR-221-3p inhibitor suppressed the pro-angiogenesis effect of ATV-Exos.

conclusionsExosomes originated from ATV-pretreated MSCs might serve as a potential strategy for the treatment of diabetic skin defects through enhancing the biological function of endothelial cells via AKT/eNOS pathway by upregulating the miR-221-3p.

Indexed as

Diabetes Mellitus, ExperimentalExosomesMesenchymal Stem CellsProto-Oncogene Proteins c-aktWound HealingAnimalsAtorvastatinCell ProliferationMicroRNAsNeovascularization, PhysiologicRatsVascular Endothelial Growth Factor AAtorvastatinMicroRNAsProto-Oncogene Proteins c-aktVascular Endothelial Growth Factor AAngiogenesisAtorvastatinDiabetic woundExosomeMesenchymal stem cell

Identifiers

PMID32787917
PMCPMC7425015
OpenAlexW3048723046

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.