Evidence map›Paper›PMID 41737208›Full record

ArticleFrontiers in immunology2026

Identification and histological validation of autophagy-related core genes ADRB2 and PLK2 in keloids, with integrated immune infiltration analysis.

Junjie Jin, Yue Jin, Bo Lu, Zhehu Jin

Abstract read
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Junjie JinDepartment of Dermatology, Yanbian University Hospital, Yanbian University Medical College, Yanji, China.
Yue JinDepartment of Dermatology, Yanbian University Hospital, Yanbian University Medical College, Yanji, China.
Bo LuDepartment of Dermatology, Yanbian University Hospital, Yanbian University Medical College, Yanji, China.
Zhehu JinDepartment of Dermatology, Yanbian University Hospital, Yanbian University Medical College, Yanji, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Keloids are pathological fibroproliferative scars characterized by excessive collagen deposition and a lack of effective targeted therapies. Autophagy dysregulation has been linked to keloid pathogenesis, but the underlying molecular mechanisms remain unclear. Methods: Transcriptomic datasets were integrated and analyzed using differential expression analysis and weighted gene co-expression network analysis. Three machine learning algorithms-least absolute shrinkage and selection operator (LASSO), support vector machine-recursive feature elimination (SVM-RFE), and random forest-were applied to identify autophagy-related hub gene candidates in keloids. Immune infiltration and functional analyses were conducted to explore immune microenvironment alterations. Histological staining (H&E and Masson), immunohistochemistry, and Western blotting were used for tissue-level validation, while cellular experiments were performed in keloid fibroblasts with autophagy modulation. Results: ADRB2 and PLK2 were consistently identified as key autophagy-related candidate genes. Immune-related analyses suggested that these genes may be involved in remodeling the keloid immune microenvironment by influencing the abundance and functional status of multiple immune cell subsets. Histological and protein-level assays demonstrated significantly higher expression of ADRB2 and PLK2 in keloid tissues compared with adjacent normal skin. In keloid fibroblasts, fibrotic markers (COL1/COL3) and autophagy-related markers (LC3-II/LC3-I and p62) were upregulated concomitantly with ADRB2 and PLK2 at baseline. Autophagy modulation altered ADRB2 expression (decreased with EBSS and increased with chloroquine), whereas PLK2 expression remained largely unchanged. Discussion: These findings identify ADRB2 and PLK2 as under-recognized autophagy- andimmunity-related candidate biomarkers in keloids, highlighting their potential relevance asdiagnostic indicators and future therapeutic research targets.

Indexed as

AutophagyKeloidProtein Serine-Threonine KinasesReceptors, Adrenergic, beta-2BiomarkersCells, CulturedFibroblastsHumansADRB2 protein, humanBiomarkersPLK2 protein, humanProtein Serine-Threonine KinasesReceptors, Adrenergic, beta-2ADRB2autophagyimmune microenvironmentkeloidPLK2

Identifiers

PMID41737208
PMCPMC12926160

What Socratic holds

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Registered trials

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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 Socratic graph.