ArticleFrontiers in molecular biosciences2026
Exploring hub genes related to adipocytokines in keloids: a combined analysis integrating single-cell, Mendelian randomization and bulk transcriptome data with experimental verification.
Article in Frontiers in molecular biosciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Keloids are fibroproliferative skin tumors with excessive collagen deposition and are strongly linked to adipocytokine dysregulation. However, the underlying mechanisms remain unclear. This study aimed to identify potential therapeutic targets and elucidate adipocytokine-related pathological mechanisms underlying keloid formation. Methods: Hub genes were identified using differential expression analysis and machine learning. Mendelian randomization assessed causal relationships. Functional insights were gained through gene set enrichment analysis (GSEA) and drug prediction. Single-cell RNA sequencing (scRNA-seq) identified key cell types, and RT-qPCR validated gene expression. Results: We identified 818 differentially expressed genes, narrowing to seven key genes and two hub genes: PIK3R3 and ANGPTL5. MR indicated PIK3R3 as a causal risk factor for keloids, while ANGPTL5 showed no causal association. GSEA linked PIK3R3 to the TEL pathway and ANGPTL5 to adipocyte differentiation. Drug predictions included harmine for PIK3R3 and silica for ANGPTL5. scRNA-seq highlighted fibroblasts as key cells expressing these genes. RT-qPCR confirmed PIK3R3 upregulation in keloids, though ANGPTL5 results were inconsistent, possibly due to sample limitations. Conclusion: This study, based on the integrated re-analysis of existing publicly available transcriptomic data and combined with clinical sample validation, revealed the potential hub roles of PIK3R3 and ANGPTL5 in keloid pathogenesis. PIK3R3 was validated as a causal hub gene, while ANGPTL5 also showed relevance. The study provides new molecular evidence and mechanistic insights for understanding the adipocytokine-related pathological mechanisms of keloids, and suggests potential therapeutic directions such as harmine for future research.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.