ArticleStem cells and development2023
AMPK Regulates DNA Methylation of PGC-1α and Myogenic Differentiation in Human Mesenchymal Stem Cells.
Article in Stem cells and development, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Molecular Hydrogen as a Regulator of Mitochondrial Quality Control and Metabolic Reprogramming.International journal of molecular sciences · 2026Review
- Emerging roles of epigenetics in the pathogenesis of sarcopenia.Epigenomics · 2026Review
- Gestational Diabetes Exposed Mesenchymal Stem Cells: Phenotypic Differences Link to Long-Term Health of Offspring.International journal of molecular sciences · 2025Review
- The Crucial Role of Epigenetic Modifications in Wharton's Jelly Stem Cells.International journal of molecular sciences · 2025Review
- AMPK is necessary for Treg functional adaptation to microenvironmental stress during malignancy and viral pneumonia.The Journal of clinical investigation · 2025Article
- Sirt2 deficiency aggravates intramuscular adipose tissue infiltration and impairs myogenesis with aging in male mice.Biogerontology · 2025Article
- AMP-activated protein kinase activation suppresses leptin expression independently of adipogenesis in primary murine adipocytes.The Biochemical journal · 2024Article
- AMP-activated protein kinase is necessary for Treg cell functional adaptation to microenvironmental stress.bioRxiv : the preprint server for biology · 2023Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Adverse intrauterine environments can cause persistent changes in epigenetic profiles of stem cells, increasing susceptibility of the offspring to developing metabolic diseases later in life. Effective approaches to restore the epigenetic landscape and function of stem cells remain to be determined. In this study, we investigated the effects of pharmaceutical activation of AMP-activated protein kinase (AMPK), an essential regulator of energy metabolism, on mitochondrial programming of Wharton's Jelly mesenchymal stem cells (WJ-MSCs) from women with diabetes during pregnancy. Induction of myogenic differentiation of WJ-MSCs was associated with increased proliferator-activated receptor-γ coactivator-1α (PGC-1α) expression and mitochondrial DNA (mtDNA) abundance. Inhibition of DNA methylation by 5 Azacytidine significantly increased PGC-1α expression and mtDNA abundance in WJ-MSCs, which were abolished by AMPK inhibitor Compound C (CC), suggesting an AMPK-dependent role of DNA demethylation in regulating mitochondrial biogenesis in WJ-MSCs. Furthermore, activation of AMPK in diabetic WJ-MSCs by AICAR or metformin decreased the level of PGC-1α promoter methylation and increased PGC-1α expression. Notably, decreased PGC-1α promoter methylation by transient treatment of AMPK activators persisted after myogenic differentiation. This was associated with enhanced myogenic differentiation capacity of human WJ-MSCs and increased mitochondrial function. Taken together, our findings revealed an important role for AMPK activators in epigenetic regulation of mitochondrial biogenesis and myogenesis in WJ-MSCs, which could lead to potential therapeutics for preventing fetal mitochondrial programming and long-term adverse outcome in offspring of women with diabetes during pregnancy.
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