Evidence map›Paper›PMID 33396192›Full record

ArticleGenes2020

Transcriptomic Analysis of a Diabetic Skin-Humanized Mouse Model Dissects Molecular Pathways Underlying the Delayed Wound Healing Response.

Carlos León, Francisco García-García, Sara Llames, Eva García-Pérez, Marta Carretero, María Del Carmen Arriba, Joaquín Dopazo, Marcela Del Río, María José Escámez, Lucía Martínez-Santamaría

Abstract read
In one paragraph

Article in Genes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. A Review of Genes Involved in Wound Healing.Medical journal of the Islamic Republic of Iran · 2023
    Review
  10. Article
  11. Article
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

10 authors.

Carlos LeónDepartment of Bioengineering, Carlos III University, Av. de la Universidad, 30, Leganés, 28911 Madrid, Spain.
Francisco García-GarcíaBioinformatics and Biostatistics Unit, Prince Felipe Research Center (CIPF), C/Eduardo Primo Yúfera, 3, 46012 Valencia, Spain.
Sara LlamesNetwork Research on Rare Diseases (CIBERER), U714, C/Melchor Fernández Almagro, 3, 28029 Madrid, Spain.ORCID 0000-0001-5456-1389
Eva García-PérezTissue Engineering Unit, Blood and Tissue Community Center of Asturias (CCST), C/Emilio Rodríguez Vigil s/n, 33006 Oviedo, Spain.ORCID 0000-0002-3594-9318
Marta CarreteroNetwork Research on Rare Diseases (CIBERER), U714, C/Melchor Fernández Almagro, 3, 28029 Madrid, Spain.
María Del Carmen ArribaDepartment of Bioengineering, Carlos III University, Av. de la Universidad, 30, Leganés, 28911 Madrid, Spain.
Joaquín DopazoClinical Bioinformatics Research Area, Progress and Health Foundation (FPS), CDCA, Hospital Virgen del Rocío, Av. Manuel Siurot s/n, 41013 Sevilla, Spain.ORCID 0000-0003-3318-120X
Marcela Del RíoDepartment of Bioengineering, Carlos III University, Av. de la Universidad, 30, Leganés, 28911 Madrid, Spain.
María José EscámezDepartment of Bioengineering, Carlos III University, Av. de la Universidad, 30, Leganés, 28911 Madrid, Spain.ORCID 0000-0002-5434-1885
Lucía Martínez-SantamaríaDepartment of Bioengineering, Carlos III University, Av. de la Universidad, 30, Leganés, 28911 Madrid, Spain.ORCID 0000-0002-9637-2364

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defective healing leading to cutaneous ulcer formation is one of the most feared complications of diabetes due to its consequences on patients' quality of life and on the healthcare system. A more in-depth analysis of the underlying molecular pathophysiology is required to develop effective healing-promoting therapies for those patients. Major architectural and functional differences with human epidermis limit extrapolation of results coming from rodents and other small mammal-healing models. Therefore, the search for reliable humanized models has become mandatory. Previously, we developed a diabetes-induced delayed humanized wound healing model that faithfully recapitulated the major histological features of such skin repair-deficient condition. Herein, we present the results of a transcriptomic and functional enrichment analysis followed by a mechanistic analysis performed in such humanized wound healing model. The deregulation of genes implicated in functions such as angiogenesis, apoptosis, and inflammatory signaling processes were evidenced, confirming published data in diabetic patients that in fact might also underlie some of the histological features previously reported in the delayed skin-humanized healing model. Altogether, these molecular findings support the utility of such preclinical model as a valuable tool to gain insight into the molecular basis of the delayed diabetic healing with potential impact in the translational medicine field.

Indexed as

TranscriptomeAnimalsDiabetes Mellitus, ExperimentalGene Expression ProfilingGene Expression RegulationGene OntologyHumansMetabolic Networks and PathwaysMiceMice, NudeMicroarray AnalysisMolecular Sequence AnnotationPrincipal Component AnalysisSignal TransductionSkinSkin TransplantationStreptozocindiabetesenrichment analysisskin-humanized micetranscriptomicswound healing

Identifiers

PMID33396192
PMCPMC7824036

What Socratic holds

Textmetadata
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 Socratic graph.