Evidence map›Paper›PMID 34065916›Full record

ReviewInternational journal of molecular sciences2021

Impaired Wound Healing, Fibrosis, and Cancer: The Paradigm of Recessive Dystrophic Epidermolysis Bullosa.

Grace Tartaglia, Qingqing Cao, Zachary M Padron, Andrew P South

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 41 citations in OpenAlex.

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  17. The two sides of chromosomal instability: drivers and brakes in cancer.Signal transduction and targeted therapy · 2024
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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

4 authors at 1 institution in 1 country.

Grace TartagliaDepartment of Dermatology and Cutaneous Biology, Thomas Jefferson University, 233 S. 10th Street, BLSB 406, Philadelphia, PA 19107, USA.ORCID 0000-0002-1403-7010
Qingqing CaoDepartment of Dermatology and Cutaneous Biology, Thomas Jefferson University, 233 S. 10th Street, BLSB 406, Philadelphia, PA 19107, USA.ORCID 0000-0001-6067-8209
Zachary M PadronDepartment of Dermatology and Cutaneous Biology, Thomas Jefferson University, 233 S. 10th Street, BLSB 406, Philadelphia, PA 19107, USA.
Andrew P SouthDepartment of Dermatology and Cutaneous Biology, Thomas Jefferson University, 233 S. 10th Street, BLSB 406, Philadelphia, PA 19107, USA.
Thomas Jefferson University · US

Funding

Training in Tissue Engineering and Regenerative MedicineT32AR052273 · NIAMS · THOMAS JEFFERSON UNIVERSITY · PI SHAPIRO, IRVING M · 2006 to 2020
$3.3M
Tissue Damage-Driven Squamous Cell CarcinomaR01CA244522 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI SOUTH, ANDREW · 2021 to 2025
$1.7M
NCI NIH HHS R01 CA244522NIAMS NIH HHS 5T32AR052273Office of the Assistant Secretary for Health W81XWH-16-1-0679Office of the Assistant Secretary for Health W81XWH-18-1-0382
6 · The paper itself

Abstract

Recessive Dystrophic Epidermolysis Bullosa (RDEB) is a devastating skin blistering disease caused by mutations in the gene encoding type VII collagen (C7), leading to epidermal fragility, trauma-induced blistering, and long term, hard-to-heal wounds. Fibrosis develops rapidly in RDEB skin and contributes to both chronic wounds, which emerge after cycles of repetitive wound and scar formation, and squamous cell carcinoma-the single biggest cause of death in this patient group. The molecular pathways disrupted in a broad spectrum of fibrotic disease are also disrupted in RDEB, and squamous cell carcinomas arising in RDEB are thus far molecularly indistinct from other sub-types of aggressive squamous cell carcinoma (SCC). Collectively these data demonstrate RDEB is a model for understanding the molecular basis of both fibrosis and rapidly developing aggressive cancer. A number of studies have shown that RDEB pathogenesis is driven by a radical change in extracellular matrix (ECM) composition and increased transforming growth factor-beta (TGFβ) signaling that is a direct result of C7 loss-of-function in dermal fibroblasts. However, the exact mechanism of how C7 loss results in extensive fibrosis is unclear, particularly how TGFβ signaling is activated and then sustained through complex networks of cell-cell interaction not limited to the traditional fibrotic protagonist, the dermal fibroblast. Continued study of this rare disease will likely yield paradigms relevant to more common pathologies.

Indexed as

Signal TransductionCarcinoma, Squamous CellCollagen Type VIIEpidermolysis Bullosa DystrophicaExtracellular MatrixFibrosisGene Expression Regulation, NeoplasticHumansMutationSkin NeoplasmsTransforming Growth Factor betaWound HealingCOL7A1 protein, humanCollagen Type VIITransforming Growth Factor betafibrosisrecessive dystrophic epidermolysis bullosasquamous cell carcinomatherapieswound healing

Identifiers

PMID34065916
PMCPMC8151646
OpenAlexW3163780706

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.