ArticleAging cell2024
Transcriptome-wide analysis reveals GYG2 as a mitochondria-related aging biomarker in human subcutaneous adipose tissue.
Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- MCPB-21 targets glycogenin-2 to regulate fatty acid oxidation and promote ferroptosis of breast cancer.American journal of cancer research · 2026Article
- Energy Metabolic Regulatory Materials Promote Wound Healing in Senescent Environment.Progress in molecular and subcellular biology · 2026Review
- Article
- Human glycogenins maintain glucose homeostasis by regulating glycogen metabolism.Nature communications · 2025Article
- Mitochondrial medicine: "from bench to bedside" 3PM-guided concept.The EPMA journal · 2025Article
- Transcriptome-wide analysis reveals GYG2 as a mitochondria-related aging biomarker in human subcutaneous adipose tissue.Aging cell · 2024Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Subcutaneous adipose tissue (SAT), a vital energy reservoir and endocrine organ for maintaining systemic glucose, lipid, and energy homeostasis, undergoes significant changes with age. However, among the existing aging-related markers, only few genes are associated with SAT aging. In this study, weighted gene co-expression network analysis was used on a transcriptome of SAT obtained from the Genotype-Tissue Expression portal to identify biologically relevant, SAT-specific, and age-related marker genes. We found modules that exhibited significant changes with age and identified GYG2 as a novel key aging associated gene. The link between GYG2 and mitochondrial function as well as brown/beige adipocytes was supported using additional bioinformatics and experimental analyses. Additionally, we identified PPARG as the transcription factor of GYG2 expression. The newly discovered GYG2 marker can be used to not only determine the age of SAT but also uncover new mechanisms underlying SAT aging.
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Registered trials
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