Evidence map›Paper›PMID 30392877›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2019

Targeting epigenetic mechanisms in diabetic wound healing.

Aaron den Dekker, Frank M Davis, Steve L Kunkel, Katherine A Gallagher

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 3 pooled it
9.0field-weighted citation impact, top 2% 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

119 citing papers in PubMed, 3 syntheses or guidelines pooled it, 224 citations in OpenAlex.

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59 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

4 authors at 1 institution in 1 country.

Aaron den DekkerDepartment of Surgery, University of Michigan, Ann Arbor, Michgan.
Frank M DavisDepartment of Surgery, University of Michigan, Ann Arbor, Michgan.
Steve L KunkelDepartment of Pathology, University of Michigan, Ann Arbor, Michigan.
Katherine A GallagherDepartment of Surgery, University of Michigan, Ann Arbor, Michgan. Electronic address: kgallag@med.umich.edu.
University of Michigan–Ann Arbor · US

Funding

Michigan Institute for Clinical and Health Research (MICHR)UL1TR002240 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUMENG, JULIE C, MASHOUR, GEORGE ALEXANDER · 2017 to 2022
$54.9M
Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
MONOKINE GENE EXPRESSION/REGULATION IN LUNG INJURYR01HL031237 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KUNKEL, STEVEN LYNN, STANDIFORD, THEODORE J. · 1985 to 2017
$5.9M
NIDDK Diabetic Foot Consortium Clinical Research UnitU01DK119083 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RODICA BUSUI (POP-BUSUI), Crystal Murray Holmes · 2018 to 2026
$5.5M
The Interferon-beta (IFN-beta)/SETDB2 Epigenetic Axis Regulates Inflammation And Metabolism In Diabetic WoundsR01HL137919 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GALLAGHER, KATHERINE ANN · 2017 to 2021
$2.4M
NCATS NIH HHS UL1 TR002240NHLBI NIH HHS R01 HL031237NHLBI NIH HHS R01 HL137919NIDDK NIH HHS P30 DK020572NIDDK NIH HHS U01 DK119083
6 · The paper itself

Abstract

Impaired wound healing is a major secondary complication of type 2 diabetes that often results in limb loss and disability. Normal tissue repair progresses through discrete phases including hemostasis, inflammation, proliferation, and remodeling. In diabetes, normal progression through these phases is impaired resulting in a sustained inflammatory state and dysfunctional epithelialization in the wound. Due to their plasticity, macrophages play a critical role in the transition from the inflammation phase to the proliferation phase. Diabetes disrupts macrophage function by impairing monocyte recruitment to the wound, reducing phagocytosis, and prohibiting the transition of inflammatory macrophages to an anti-inflammatory state. Diabetes also impedes keratinocyte and fibroblast function during the later phases resulting in impaired epithelialization of the wound. Several recent studies suggest that altered epigenetic regulation of both immune and structural cells in wounds may influence cell phenotypes and healing, particularly in pathologic states, such as diabetes. Specifically, it has been shown that macrophage plasticity during wound repair is partly regulated epigenetically and that diabetes alters this epigenetic regulation and contributes to a sustained inflammatory state. Epigenetic regulation is also known to regulate keratinocyte and fibroblast function during wound repair. In this review, we provide an introduction to the epigenetic mechanisms that regulate tissue repair and highlight recent findings that demonstrate, how epigenetic events are altered during the course of diabetic wound healing.

Indexed as

Epigenesis, GeneticAnimalsCell PlasticityChromatin Assembly and DisassemblyDiabetes Mellitus, Type 2Diabetic FootDNA MethylationFibroblastsHistonesHumansMacrophagesWound HealingHistones

Identifiers

PMID30392877
PMCPMC6331222
OpenAlexW2896818937

What OpenQuestion holds

Textmetadata
LicenceTDM
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.