Evidence map›Paper›PMID 32167156›Full record

ArticleBritish journal of pharmacology2020

Low-concentration DMSO accelerates skin wound healing by Akt/mTOR-mediated cell proliferation and migration in diabetic mice.

Wei Guo, Wei Qiu, Xiang Ao, Weiqiang Li, Xiao He, Luoquan Ao, Xueting Hu, Zhan Li, Ming Zhu, Donglin Luo and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

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  3. Preparation and Investigation ofPharmaceuticals (Basel, Switzerland) · 2026
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  20. Correction.British journal of pharmacology · 2020
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

Wei GuoDepartment of Stem Cell & Regenerative Medicine.
Wei QiuDepartment of Stem Cell & Regenerative Medicine.
Xiang AoDepartment of Stem Cell & Regenerative Medicine.
Weiqiang LiDepartment of Stem Cell & Regenerative Medicine.
Xiao HeDepartment of Stem Cell & Regenerative Medicine.
Luoquan AoDepartment of Stem Cell & Regenerative Medicine.
Xueting HuDepartment of Stem Cell & Regenerative Medicine.
Zhan LiDepartment of Stem Cell & Regenerative Medicine.
Ming ZhuDepartment of Stem Cell & Regenerative Medicine.
Donglin LuoDepartment of General Surgery, Daping Hospital, Army Medical University, Chongqing, P.R. China.
Wei XingDepartment of Stem Cell & Regenerative Medicine.
Xiang XuDepartment of Stem Cell & Regenerative Medicine.
Daping Hospital · CNArmy Medical University · CNChongqing Medical University · CN

Funding

Chongqing Natural Science Foundation cstc2015jcyjA10078Military pre-research program of the Army Medical University 2019XYY21National Natural Science Foundation of China 81571913National Natural Science Foundation of China 81871568
6 · The paper itself

Abstract

background and purposeDMSO has been found to promote tissue repair. However, the role of DMSO in diabetic skin wound healing and the underlying molecular mechanisms are still unclear. EXPERIMENTAL APPROACH: The effects of DMSO on wound healing were evaluated by HE staining, immunohistochemistry and collagen staining using a wound model of full-thickness skin resection on the backs of non-diabetic or diabetic mice. Real-time cell analysis and 5-ethynyl-2'-deoxyuridine incorporation assays were used to study the effect of DMSO on primary fibroblast proliferation. A transwell assay was used to investigate keratinocyte migration. The associated signalling pathway was identified by western blotting and inhibitor blocking. The effect of DMSO on the translation rate of downstream target genes was studied by RT-qPCR of polyribosome mRNA. KEY

resultsWe found that low-concentration DMSO significantly accelerated skin wound closure by promoting fibroblast proliferation in both nondiabetic and diabetic mice. In addition, increased migration of keratinocytes may also contribute to accelerated wound healing, which was stimulated by increased TGF-β1 secretion from fibroblasts. Furthermore, we demonstrated that this effect of DMSO depends on Akt/mTOR-mediated translational control and the promotion of the translation of a set of cell proliferation-related genes. As expected, DMSO-induced wound healing and cell proliferation were impaired by rapamycin, an inhibitor of Akt/mTOR signalling. CONCLUSION AND IMPLICATIONS: DMSO can promote skin wound healing in diabetic mice by activating the Akt/mTOR pathway. Low-concentration DMSO presents an alternative medication for chronic cutaneous wounds, especially for diabetic patients.

Indexed as

Diabetes Mellitus, ExperimentalProto-Oncogene Proteins c-aktAnimalsCell MovementCell ProliferationDimethyl SulfoxideFibroblastsHumansMiceSkinTOR Serine-Threonine KinasesWound HealingDimethyl SulfoxideMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID32167156
PMCPMC7312275
OpenAlexW3011975585

What OpenQuestion holds

Textmetadata
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.