Evidence map›Paper›PMID 37122894›Full record

ArticleBioactive materials2023

Novel neutrophil extracellular trap-related mechanisms in diabetic wounds inspire a promising treatment strategy with hypoxia-challenged small extracellular vesicles.

Ziqiang Chu, Qilin Huang, Kui Ma, Xi Liu, Wenhua Zhang, Shengnan Cui, Qian Wei, Huanhuan Gao, Wenzhi Hu, Zihao Wang and 5 more

Open access · goldAbstract read
In one paragraph

Article in Bioactive materials, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 2 pooled it
13.7field-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

54 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

  1. Pooled it
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  5. MMP8 Promotes NETosis in Gestational Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2026
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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

15 authors at 4 institutions in 1 country.

Ziqiang ChuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Qilin HuangCollege of Graduate, Tianjin Medical University, Tianjin, 300070, PR China.
Kui MaResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Xi LiuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Wenhua ZhangResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Shengnan CuiResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Qian WeiResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Huanhuan GaoResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Wenzhi HuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Zihao WangResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Sheng MengResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Lige TianCollege of Graduate, Tianjin Medical University, Tianjin, 300070, PR China.
Haihong LiDepartment of Wound Repair, Institute of Wound Repair and Regeneration Medicine, Southern University of Science and Technology Hospital, Southern University of Science and Technology School of Medicine, Shenzhen, 518055, PR China.
Xiaobing FuResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Cuiping ZhangResearch Center for Tissue Repair and Regeneration Affiliated to the Medical Innovation Research Department, PLA General Hospital, 28 Fuxing Road, Beijing, 100853, PR China.
Chinese PLA General Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNTianjin Medical University · CNSouthern University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophil extracellular traps (NETs) have been considered a significant unfavorable factor for wound healing in diabetes, but the mechanisms remain unclear. The therapeutic application of small extracellular vesicles (sEVs) derived from mesenchymal stem cells (MSCs) has received considerable attention for their properties. Hypoxic preconditioning is reported to enhance the therapeutic potential of MSC-derived sEVs in regenerative medicine. Therefore, the aim of this study is to illustrate the detailed mechanism of NETs in impairment of diabetic wound healing and develop a promising NET-targeting treatment based on hypoxic pretreated MSC-derived sEVs (Hypo-sEVs). Excessive NETs were found in diabetic wounds and in high glucose (HG)-induced neutrophils. Further research showed that high concentration of NETs impaired the function of fibroblasts through activating endoplasmic reticulum (ER) stress. Hypo-sEVs efficiently promoted diabetic wound healing and reduced the excessive NET formation by transferring miR-17-5p. Bioinformatic analysis and RNA interference experiment revealed that miR-17-5p in Hypo-sEVs obstructed the NET formation by targeting TLR4/ROS/MAPK pathway. Additionally, miR-17-5p overexpression decreased NET formation and overcame NET-induced impairment in fibroblasts, similar to the effects of Hypo-sEVs. Overall, we identify a previously unrecognized NET-related mechanism in diabetic wounds and provide a promising NET-targeting strategy for wound treatment.

Indexed as

Diabetic wound healingEndoplasmic reticulum stressHypoxiaNeutrophil extracellular trapsSmall extracellular vesicles

Identifiers

PMID37122894
PMCPMC10133407
OpenAlexW4365520033

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.