Evidence map›Paper›PMID 34443506›Full record

ReviewMolecules (Basel, Switzerland)2021

Skin Wound Healing: Normal Macrophage Function and Macrophage Dysfunction in Diabetic Wounds.

Savannah M Aitcheson, Francesca D Frentiu, Sheree E Hurn, Katie Edwards, Rachael Z Murray

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 231 papers.

0numbers the graph read from it
0cells of the map it votes in
231citing papers in PubMed
27.7field-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

231 citing papers in PubMed, 397 citations in OpenAlex.

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  11. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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171 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

5 authors at 1 institution in 1 country.

Savannah M AitchesonSchool of Biomedical Sciences and Centre for Immunology and Infection Control, Faculty of Health, Queensland University of Technology, Brisbane, QLD 4059, Australia.ORCID 0000-0002-8452-4711
Francesca D FrentiuSchool of Biomedical Sciences and Centre for Immunology and Infection Control, Faculty of Health, Queensland University of Technology, Brisbane, QLD 4059, Australia.ORCID 0000-0001-8628-4216
Sheree E HurnSchool of Clinical Sciences, Faculty of Health, Queensland University of Technology, Brisbane, QLD 4059, Australia.
Katie EdwardsSchool of Optometry and Vision Science, Faculty of Health, Queensland University of Technology, Brisbane, QLD 4059, Australia.
Rachael Z MurraySchool of Biomedical Sciences and Centre for Immunology and Infection Control, Faculty of Health, Queensland University of Technology, Brisbane, QLD 4059, Australia.ORCID 0000-0002-4935-7794
Queensland University of Technology · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages play a prominent role in wound healing. In the early stages, they promote inflammation and remove pathogens, wound debris, and cells that have apoptosed. Later in the repair process, they dampen inflammation and secrete factors that regulate the proliferation, differentiation, and migration of keratinocytes, fibroblasts, and endothelial cells, leading to neovascularisation and wound closure. The macrophages that coordinate this repair process are complex: they originate from different sources and have distinct phenotypes with diverse functions that act at various times in the repair process. Macrophages in individuals with diabetes are altered, displaying hyperresponsiveness to inflammatory stimulants and increased secretion of pro-inflammatory cytokines. They also have a reduced ability to phagocytose pathogens and efferocytose cells that have undergone apoptosis. This leads to a reduced capacity to remove pathogens and, as efferocytosis is a trigger for their phenotypic switch, it reduces the number of M2 reparative macrophages in the wound. This can lead to diabetic foot ulcers (DFUs) forming and contributes to their increased risk of not healing and becoming infected, and potentially, amputation. Understanding macrophage dysregulation in DFUs and how these cells might be altered, along with the associated inflammation, will ultimately allow for better therapies that might complement current treatment and increase DFU's healing rates.

Indexed as

Wound HealingAnimalsDiabetes MellitusHumansInflammationMacrophagesModels, BiologicalSkinchronic wounddiabetic foot ulcerefferocytosisinfectioninflammationmacrophagephenotype

Identifiers

PMID34443506
PMCPMC8398285
OpenAlexW3195937928

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.