Evidence map›Paper›PMID 31465751›Full record

ArticleThe American journal of pathology2019

Tissue Iron Promotes Wound Repair via M2 Macrophage Polarization and the Chemokine (C-C Motif) Ligands 17 and 22.

Holly N Wilkinson, Elizabeth R Roberts, Amber R Stafford, Kayleigh L Banyard, Paolo Matteucci, Kimberly A Mace, Matthew J Hardman

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 76 citations in OpenAlex.

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  13. Macrophage heterogeneity in liver fibrosis.Frontiers in immunology · 2025
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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

7 authors at 3 institutions in 1 country.

Holly N WilkinsonCentre for Atherothrombosis and Metabolic Disease, Hull York Medical School, University of Hull, Hull.
Elizabeth R RobertsCentre for Atherothrombosis and Metabolic Disease, Hull York Medical School, University of Hull, Hull.
Amber R StaffordCentre for Atherothrombosis and Metabolic Disease, Hull York Medical School, University of Hull, Hull.
Kayleigh L BanyardCentre for Atherothrombosis and Metabolic Disease, Hull York Medical School, University of Hull, Hull.
Paolo MatteucciHull and East Yorkshire Hospitals National Health Service Trust, Hull.
Kimberly A MaceFaculty of Biology, Medicine and Health, The University of Manchester, Manchester, United Kingdom.
Matthew J HardmanCentre for Atherothrombosis and Metabolic Disease, Hull York Medical School, University of Hull, Hull. Electronic address: m.hardman@hull.ac.uk.
University of Hull · GBNational Health Service · GBUniversity of Manchester · GB

Funding

Medical Research Council MR/L010267/1Medical Research Council MR/L010267/2Medical Research Council MR/M016307/1
6 · The paper itself

Abstract

Macrophages are important for effective iron recycling and erythropoiesis, but they also play a crucial role in wound healing, orchestrating tissue repair. Recently, we demonstrated a significant accumulation of iron in healing wounds and a requirement of iron for effective repair. Herein, we sought to determine the influence of iron on macrophage function in the context of wound healing. Interestingly, wound macrophages extensively sequestered iron throughout healing, associated with a prohealing M2 phenotype. In delayed healing diabetic mouse wounds, both macrophage polarization and iron sequestration were impaired. In vitro studies revealed that iron promotes differentiation, while skewing macrophages toward a hypersecretory M2-like polarization state. These macrophages produced high levels of chemokine (C-C motif) ligands 17 and 22, promoting wound reepithelialization and extracellular matrix deposition in a human ex vivo wound healing model. Together, these findings reveal a novel, unappreciated role for iron in modulating macrophage behavior to promote subsequent wound repair. These findings support therapeutic evaluation of iron use to promote wound healing in the clinic.

Indexed as

AnimalsCell DifferentiationCell PolarityCells, CulturedChemokine CCL17Chemokine CCL22Diabetes Mellitus, ExperimentalDisease Models, AnimalFemaleHumansIronMacrophage ActivationMacrophagesMiceMice, Inbred C57BLMice, TransgenicCCL17 protein, humanCCL22 protein, humanChemokine CCL17Chemokine CCL22Ironleptin receptor, mouseReceptors, Leptin

Identifiers

PMID31465751
PMCPMC12179499
OpenAlexW2970860517

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.