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Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE293139 | GEO | 2025/10/15

REPOSITORIES: GEO

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Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [Hi-C]

Project description:Loss of regeneration is a key feature of aging organs, often linked to stem cell exhaustion. Skeletal muscle stem cells (MuSCs) undergo age-related numerical and functional decline, contributing to reduced regenerative potential. Using low-input multi-omics, we systematically profiled the epigenome, transcriptome, and 3D genome of MuSCs from individual mice across 3 age groups (young, old, and geriatric) and both sexes. MuSCs from aged mice, particularly males, exhibited early alterations (evident in old), including enhanced proinflammatory signaling with loss of cell identity. Late alterations (evident in geriatric) included heightened inflammation, widespread enhancer activation, and 3D genome rewiring. Proinflammatory pathways were enriched for interferon signaling and correlated with endogenous retroviral expression and NFκB activity. Late-stage epigenome and 3D genome rewiring reflected downstream degenerative changes in muscle organization, response to cytokines, and loss of myogenic identity. These progressive molecular shifts may explain the aggravated proliferative deficit observed in MuSCs during aging.

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Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [RNA-seq]

Project description:Loss of regeneration is a key feature of aging organs, often linked to stem cell exhaustion. Skeletal muscle stem cells (MuSCs) undergo age-related numerical and functional decline, contributing to reduced regenerative potential. Using low-input multi-omics, we systematically profiled the epigenome, transcriptome, and 3D genome of MuSCs from individual mice across 3 age groups (young, old, and geriatric) and both sexes. At baseline, young male MuSCs showed reduced expression of cell cycle-related mRNAs. In aged mice, particularly males, MuSCs exhibited early alterations (emerging during the transition from young to old age), including enhanced proinflammatory signaling, and loss of cell identity. Late alterations (emerging during the transition from old to geriatric age) included heightened inflammation, widespread enhancer activation, and extensive 3D genome rewiring. Proinflammatory pathways were enriched for interferon signaling and correlated with endogenous retroviral expression and NFκB activity. Late-stage epigenome and 3D genome rewiring reflected downstream degenerative changes in muscle organization, response to cytokines, and loss of myogenic identity. Thus, progressive molecular shifts may explain the aggravated proliferative deficit and functional impairment observed in MuSCs during aging.

2025-11-13 | GSE293130 | GEO

Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [CUT&RUN]

Project description:Loss of regeneration is a key feature of aging organs, often linked to stem cell exhaustion. Skeletal muscle stem cells (MuSCs) undergo age-related numerical and functional decline, contributing to reduced regenerative potential. Using low-input multi-omics, we systematically profiled the epigenome, transcriptome, and 3D genome of MuSCs from individual mice across 3 age groups (young, old, and geriatric) and both sexes. At baseline, young male MuSCs showed reduced expression of cell cycle-related mRNAs. In aged mice, particularly males, MuSCs exhibited early alterations (emerging during the transition from young to old age), including enhanced proinflammatory signaling, and loss of cell identity. Late alterations (emerging during the transition from old to geriatric age) included heightened inflammation, widespread enhancer activation, and extensive 3D genome rewiring. Proinflammatory pathways were enriched for interferon signaling and correlated with endogenous retroviral expression and NFκB activity. Late-stage epigenome and 3D genome rewiring reflected downstream degenerative changes in muscle organization, response to cytokines, and loss of myogenic identity. Thus, progressive molecular shifts may explain the aggravated proliferative deficit and functional impairment observed in MuSCs during aging.

2025-11-13 | GSE293129 | GEO

Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [ATAC-seq]

Project description:Loss of regeneration is a key feature of aging organs, often linked to stem cell exhaustion. Skeletal muscle stem cells (MuSCs) undergo age-related numerical and functional decline, contributing to reduced regenerative potential. Using low-input multi-omics, we systematically profiled the epigenome, transcriptome, and 3D genome of MuSCs from individual mice across 3 age groups (young, old, and geriatric) and both sexes. At baseline, young male MuSCs showed reduced expression of cell cycle-related mRNAs. In aged mice, particularly males, MuSCs exhibited early alterations (emerging during the transition from young to old age), including enhanced proinflammatory signaling, and loss of cell identity. Late alterations (emerging during the transition from old to geriatric age) included heightened inflammation, widespread enhancer activation, and extensive 3D genome rewiring. Proinflammatory pathways were enriched for interferon signaling and correlated with endogenous retroviral expression and NFκB activity. Late-stage epigenome and 3D genome rewiring reflected downstream degenerative changes in muscle organization, response to cytokines, and loss of myogenic identity. Thus, progressive molecular shifts may explain the aggravated proliferative deficit and functional impairment observed in MuSCs during aging.

2025-11-13 | GSE293128 | GEO

Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging

Project description:Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging

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Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [RNA-seq]

Project description:Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [RNA-seq]

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Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [ATAC-seq]

Project description:Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [ATAC-seq]

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Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [Hi-C]

Project description:Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [Hi-C]

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Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [CUT&RUN]

Project description:Enhancer rewiring orchestrates inflammation and loss of cell identity during muscle stem cell aging [CUT&RUN]

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Rewiring of the promoter-enhancer interactome and regulatory landscape in glioblastoma orchestrates gene expression underlying neurogliomal synaptic communication.

Project description:Chromatin organization controls transcription by modulating 3D-interactions between enhancers and promoters in the nucleus. Alterations in epigenetic states and 3D-chromatin organization result in gene expression changes contributing to cancer. Here, we map the promoter-enhancer interactome and regulatory landscape of glioblastoma, the most aggressive primary brain tumour. Our data reveals profound rewiring of promoter-enhancer interactions, chromatin accessibility and redistribution of histone marks in glioblastoma. This leads to loss of long-range regulatory interactions and overall activation of promoters, which orchestrate changes in the expression of genes associated to glutamatergic synapses, axon guidance, axonogenesis and chromatin remodelling. SMAD3 and PITX1 emerge as major transcription factors controlling genes related to synapse organization and axon guidance. Inhibition of SMAD3 and neuronal activity stimulation cooperate to promote proliferation of glioblastoma cells in co-culture with glutamatergic neurons, and in mice bearing patient-derived xenografts. Our findings provide mechanistic insight into the regulatory networks that mediate neurogliomal synaptic communication.

| S-EPMC10576091 | biostudies-literature

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