Evidence map›Paper›PMID 33318569›Full record

ArticleCommunications biology2020

HypoxamiR-210 accelerates wound healing in diabetic mice by improving cellular metabolism.

Sampath Narayanan, Sofie Eliasson Angelstig, Cheng Xu, Jacob Grünler, Allan Zhao, Wan Zhu, Ning Xu Landén, Mona Ståhle, Jingping Zhang, Mircea Ivan and 5 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

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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 5 institutions in 4 countries.

Sampath NarayananDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Sofie Eliasson AngelstigDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Cheng XuDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Jacob GrünlerDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Allan ZhaoDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Wan ZhuDepartment of Nosocomial Infection Control, China Medical University, Shenyang, China.
Ning Xu LandénDermatology and Venereology division, Department of Medicine Solna, Center for Molecular Medicine and Ming Wai Lau Centre for Reparative Medicine, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0003-4868-3798
Mona StåhleDermatology and Venereology division, Department of Medicine Solna, Center for Molecular Medicine and Ming Wai Lau Centre for Reparative Medicine, Karolinska Institutet, Stockholm, Sweden.
Jingping ZhangDepartment of Infectious Disease, China Medical University, Shenyang, China.
Mircea IvanDepartments of Medicine, Microbiology and Immunology, Indiana University, Indianapolis, IN, USA.ORCID 0000-0003-3424-6642
Raluca Georgiana MaltesenDepartment of Anesthesia and Intensive Care Medicine, Aalborg University Hospital, Aalborg, Denmark.ORCID 0000-0003-2332-2312
Ileana Ruxandra BotusanDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Neda Rajamand EkbergDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden.
Xiaowei ZhengDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. Xiaowei.zheng@ki.se.ORCID 0000-0002-2648-1119
Sergiu-Bogdan CatrinaDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden. Sergiu-Bogdan.Catrina@ki.se.ORCID 0000-0002-6914-3902
Karolinska University Hospital · SEKarolinska Institutet · SEChina Medical University · CNAalborg University Hospital · DKIndiana University – Purdue University Indianapolis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Wound healing is a high energy demanding process that needs a good coordination of the mitochondria with glycolysis in the characteristic highly hypoxic environment. In diabetes, hyperglycemia impairs the adaptive responses to hypoxia with profound negative effects on different cellular compartments of wound healing. miR-210 is a hypoxia-induced microRNA that regulates cellular metabolism and processes important for wound healing. Here, we show that hyperglycemia blunted the hypoxia-dependent induction of miR-210 both in vitro and in human and mouse diabetic wounds. The impaired regulation of miR-210 in diabetic wounds is pathogenic, since local miR-210 administration accelerated wound healing specifically in diabetic but not in non-diabetic mice. miR-210 reconstitution restores the metabolic balance in diabetic wounds by reducing oxygen consumption rate and ROS production and by activating glycolysis with positive consequences on cellular migration. In conclusion, miR-210 accelerates wound healing specifically in diabetes through improvement of the cellular metabolism.

Indexed as

Gene Expression RegulationAnimalsBlood GlucoseCellular ReprogrammingDiabetes Mellitus, ExperimentalDisease Models, AnimalEnergy MetabolismFibroblastsHyperglycemiaHypoxiaMiceMicroRNAsWound HealingBlood GlucoseMicroRNAsMIRN210 microRNA, mouse

Identifiers

PMID33318569
PMCPMC7736285
OpenAlexW3113278288

What OpenQuestion holds

Textmetadata
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.