Evidence map›Paper›PMID 33772102›Full record

ArticleCommunications biology2021

Restoration of the healing microenvironment in diabetic wounds with matrix-binding IL-1 receptor antagonist.

Jean L Tan, Blake Lash, Rezvan Karami, Bhavana Nayer, Yen-Zhen Lu, Celeste Piotto, Ziad Julier, Mikaël M Martino

Abstract read
In one paragraph

Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

37 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Immunomodulatory Tissue-Engineering Strategies for Diabetic Foot Ulcer Management: A Systematic Review.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    Pooled it
  2. Translational development of ABCB5Stem cell research & therapy · 2022
    Trial
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  11. Sugar Functionalized Collagen Material for Local Modulation of Innate Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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  14. Observational
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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

8 authors.

Jean L Tan *European Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC, Australia.
Blake Lash *European Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC, Australia.ORCID 0000-0003-2445-7948
Rezvan KaramiEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC, Australia.
Bhavana NayerEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC, Australia.ORCID 0000-0003-4234-8630
Yen-Zhen LuEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC, Australia.
Celeste PiottoEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC, Australia.
Ziad JulierEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC, Australia.
Mikaël M MartinoEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Melbourne, VIC, Australia. mikael.martino@monash.edu.ORCID 0000-0002-5012-4605

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic wounds are a major clinical problem where wound closure is prevented by pathologic factors, including immune dysregulation. To design efficient immunotherapies, an understanding of the key molecular pathways by which immunity impairs wound healing is needed. Interleukin-1 (IL-1) plays a central role in regulating the immune response to tissue injury through IL-1 receptor (IL-1R1). Generating a knockout mouse model, we demonstrate that the IL-1-IL-1R1 axis delays wound closure in diabetic conditions. We used a protein engineering approach to deliver IL-1 receptor antagonist (IL-1Ra) in a localised and sustained manner through binding extracellular matrix components. We demonstrate that matrix-binding IL-1Ra improves wound healing in diabetic mice by re-establishing a pro-healing microenvironment characterised by lower levels of pro-inflammatory cells, cytokines and senescent fibroblasts, and higher levels of anti-inflammatory cytokines and growth factors. Engineered IL-1Ra has translational potential for chronic wounds and other inflammatory conditions where IL-1R1 signalling should be dampened.

Indexed as

AnimalsDiabetes Mellitus, ExperimentalInterleukin 1 Receptor Antagonist ProteinMaleMiceMice, KnockoutWound HealingIl1rn protein, mouseInterleukin 1 Receptor Antagonist Protein

Identifiers

PMID33772102
PMCPMC7998035

What OpenQuestion holds

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LicenceCC BY
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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.