Evidence map›Paper›PMID 39157347›Full record

ArticleHeliyon2024

Comprehensive bioinformatic analysis reveals a fibroblast-related gene signature for the diagnosis of keloids.

Yue Qi, GuiE Ma

Abstract read
In one paragraph

Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

2 authors.

Yue QiPlastic Surgery Hospital Chinese Academy of Medical Sciences, 33rd BaDaChu Street, Beijing, 100144, China.
GuiE MaPlastic Surgery Hospital Chinese Academy of Medical Sciences, 33rd BaDaChu Street, Beijing, 100144, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aim: A keloid is a fibroproliferative cutaneous disorder secondary to skin injury, caused by an imbalance in fibroblast proliferation and apoptosis. However, the pathogenesis is not fully understood. In this study, candidate genes for keloid were identified and used to construct a diagnostic model. Methods: Three datasets related to keloids were downloaded from NCBI Gene Expression Omnibus. Fibroblast-related genes were screened, and fibroblast scores for the samples were determined. Then, a weighted gene co-expression network analysis (WGCNA) was used to identify modules and genes associated with keloids and the fibroblast score. Differentially expressed genes (DEGs) between keloid and control samples were identified and compared with fibroblast-related genes and genes in the modules. Overlapping genes were evaluated using functional enrichment analyses. Signature genes were further screened, and a diagnostic model was constructed. Finally, correlations between immune cell frequences and signature genes were analyzed. Results: In total, 124 fibroblast-related genes were obtained, and the fibroblast score was an effective indicator of the sample type. WGCNA revealed five modules that were significantly correlated with both the disease state and fibroblast scores, including 1760 genes. Additionally, 589 DEGs were identified, including 16 that overlapped with fibroblast-related genes and genes identified in the WGCNA. These genes were related to cell proliferation and apoptosis and were involved in FoxO, Rap1, p53, Ras, MAPK, and PI3K-Akt pathways. Finally, a six fibroblast-related gene signature ( Conclusion: The established model based on

Indexed as

Diagnostic modelFibroblastImmune cellKeloid

Identifiers

PMID39157347
PMCPMC11327581

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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.