ArticleRedox biology2020
Epigenetic regulation of miR-29a/miR-30c/DNMT3A axis controls SOD2 and mitochondrial oxidative stress in human mesenchymal stem cells.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 60 citations in OpenAlex.
- Maternal obesity programs offspring metabolic dysfunction via small extracellular vesicle-mediated epigenetic remodeling.Nature communications · 2026Article
- Elucidating the mechanism underlying incomplete immune recovery in people living with HIV through CD4⁺ and CD8⁺ T cell multi-omics.Molecular medicine (Cambridge, Mass.) · 2026Article
- Advanced glycation end-products exacerbate myocardial ischemia/reperfusion injury by promoting mitochondrial oxidative damage and PANoptosis in diabetes mellitus.Redox biology · 2026Article
- Expression Analysis of miRNA Profiles in Colorectal Cancer with a Bioinformatics Approach: An Emphasis on miR-4295, miR-4720-5p, miR-4773, and miR-6831-5p.Diagnostics (Basel, Switzerland) · 2026Article
- Epigenetic signatures and cellular stress response pathways in metabolic dysfunction-associated steatotic liver disease: a personalized medicine perspective.Frontiers in physiology · 2026Review
- Stem cell approaches for tendon repair: delusion or insight.The Journal of physiology · 2025Review
- Mitochondrial DNA methylation is involved in contrast-induced renal tubular epithelial cell injury.Renal failure · 2025Article
- Role of Non-coding RNAs in Acute Myeloid Leukemia.Non-coding RNA · 2025Review
- miR-29a-3p and TGF-β Axis in Fanconi anemia: mechanisms driving metabolic dysfunction and genome stability.Cellular and molecular life sciences : CMLS · 2025Article
- Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.Biomedicines · 2025Review
- Dnmt3a-mediated hypermethylation of FoxO3 promotes redox imbalance during osteoclastogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cellular stress and epigenetic regulation in adult stem cells.Life science alliance · 2024Review
- Epigenetic reprogramming of mtDNA and its etiology in mitochondrial diseases.Journal of physiology and biochemistry · 2024Review
- miR-29a-3p orchestrates key signaling pathways for enhanced migration of human mesenchymal stem cells.Cell communication and signaling : CCS · 2024Article
- Multiomics profiling reveals VDR as a central regulator of mesenchymal stem cell senescence with a known association with osteoporosis after high-fat diet exposure.International journal of oral science · 2024Article
- C-Myc/H19/miR-29b axis downregulates nerve/glial (NG)2 expression in glioblastoma multiforme.Molecular therapy. Nucleic acids · 2024Article
- TRIM28-Mediated Excessive Oxidative Stress Induces Cellular Senescence in Granulosa Cells and Contributes to Premature Ovarian Insufficiency In Vitro and In Vivo.Antioxidants (Basel, Switzerland) · 2024Article
- Effect of DNA methylation on the osteogenic differentiation of mesenchymal stem cells: concise review.Frontiers in genetics · 2024Review
- Equine Hoof Progenitor Cells Display Increased Mitochondrial Metabolism and Adaptive Potential to a Highly Pro-Inflammatory Microenvironment.International journal of molecular sciences · 2023Article
- In Silico Identification of a BRCA1:miR-29:DNMT3 Axis Involved in the Control of Hormone Receptors in BRCA1-Associated Breast Cancers.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The use of human mesenchymal stem cells (hMSCs) in clinical applications requires large-scale cell expansion prior to administration. However, the prolonged culture of hMSCs results in cellular senescence, impairing their proliferation and therapeutic potentials. To understand the role of microRNAs (miRNAs) in regulating cellular senescence in hMSCs, we globally depleted miRNAs by silencing the DiGeorge syndrome critical region 8 (DGCR8) gene, an essential component of miRNA biogenesis. DGCR8 knockdown hMSCs exhibited severe proliferation defects and senescence-associated alterations, including increased levels of reactive oxygen species (ROS). Transcriptomic analysis revealed that the antioxidant gene superoxide dismutase 2 (SOD2) was significantly downregulated in DGCR8 knockdown hMSCs. Moreover, we found that DGCR8 silencing in hMSCs resulted in hypermethylation in CpG islands upstream of SOD2. 5-aza-2'-deoxycytidine treatment restored SOD2 expression and ROS levels. We also found that these effects were dependent on the epigenetic regulator DNA methyltransferase 3 alpha (DNMT3A). Using computational and experimental approaches, we demonstrated that DNMT3A expression was regulated by miR-29a-3p and miR-30c-5p. Overexpression of miR-29a-3p and/or miR-30c-5p reduced ROS levels in DGCR8 knockdown hMSCs and rescued proliferation defects, mitochondrial dysfunction, and premature senescence. Our findings provide novel insights into hMSCs senescence regulation by the miR-29a-3p/miR-30c-5p/DNMT3A/SOD2 axis.
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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.