ArticleEpigenetics & chromatin2025
Multi-omic integration of single-cell data uncovers methylation profiles of super-enhancers in skeletal muscle stem cells.
Article in Epigenetics & chromatin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- Skeletal muscle methylome-transcriptome disruptions during the onset and progression of colorectal cancer-induced cachexia.American journal of physiology. Cell physiology · 2026Article
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7 authors.
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Abstract
introductionSkeletal muscle stem cells (MuSCs) have strong regenerative abilities, but as we age, their ability to regenerate decreases, leading to a decline in muscle function. Although the methylation reprogramming of super-enhancers (SEs) plays a pivotal role in regulating gene expression associated with the aging process, our understanding of the molecular diversity of stem cells during aging remains limited. This study aimed to identify the methylation profile of SEs in MuSCs and explore potential therapeutic molecular targets associated with aging.
methodsThe ROSE software was employed to identify super enhancers from the ChIP-seq data obtained from the ENCODE database. Additionally, the ALLCools and Methylpy packages were applied to analyze the methylation profile of SEs and to identify differentially methylated regions (DMRs) between aged and control samples using single-cell bisulfite sequencing (scBS-seq) data from the Gene Expression Omnibus (GEO) database. Overlap analysis was used to assess the regions of SEs and DMRs. The target genes and motifs were analyzed using KEGG, GO, and HOMER to identify key biological pathways and functions, followed by validation through snATAC-seq and immunofluorescence techniques.
resultsIn conclusion, we conducted a multi-omics and cross-species analysis of MuSCs, creating a detailed methylation profile of SEs during aging. We identified key motifs and genes affected by SE methylation reprogramming, revealing important molecular pathways involved in aging. Notably, further analysis of the key gene PLXND1 revealed a decreasing expression trend in aged MuSCs, which appears to be linked to the hypermethylation of SE Rank 869. This epigenetic alteration is likely to contribute to the dysregulation of the SEMA3 signaling pathway, with profound implications for muscle regeneration in MuSCs during aging.
conclusionThese findings suggest that epigenetic alterations in the methylation reprogramming of SEs are closely linked to the disruption of transcriptional networks during MuSCs aging. Moreover, our results offer valuable insights into the mechanisms driving SE methylation reprogramming, shedding light on how these epigenetic changes contribute to the molecular processes underlying aging.
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