ArticleAge (Dordrecht, Netherlands)2013
SIRT3 overexpression antagonizes high glucose accelerated cellular senescence in human diploid fibroblasts via the SIRT3-FOXO1 signaling pathway.
Article in Age (Dordrecht, Netherlands), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 83 citations in OpenAlex.
- Targeting Specific Sirtuin Modulation: Emerging Therapeutic Strategies for Healthy Cognitive Ageing and Potential Implications for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2026Review
- Diabetic keratopathy and nuclear proteins (Review).Molecular medicine reports · 2026Review
- The Role of Sirt3 in Kidney Health and Disease.Pharmaceuticals (Basel, Switzerland) · 2025Review
- NRH, a potent NADMetabolism: clinical and experimental · 2025Article
- Prediction of Age-Related MicroRNA Signature in Mesenchymal Stem Cells by using Computational Methods.Current stem cell research & therapy · 2025Article
- SIRT3, a New Hope in Liver Diseases from Pathogenic Mechanisms to Therapeutic Strategies.Current pharmaceutical biotechnology · 2025Review
- A nutrigeroscience approach: Dietary macronutrients and cellular senescence.Cell metabolism · 2024Review
- Sodium Tanshinone IIA Sulfonate alleviates vascular senescence in diabetic mice by modulating the A20-NFκB-NLRP3 inflammasome-catalase pathway.Scientific reports · 2024Article
- The role of CYP-sEH derived lipid mediators in regulating mitochondrial biology and cellular senescence: implications for the aging heart.Frontiers in pharmacology · 2024Review
- LncRNA LINC01197 inhibited the formation of calcium oxalate-induced kidney stones by regulating miR-516b-5p/SIRT3/FOXO1 signaling pathway.Cell and tissue research · 2023Article
- Article
- Targeting Mitochondria to Control Ageing and Senescence.Pharmaceutics · 2023Review
- A Promising Strategy to Treat Neurodegenerative Diseases by SIRT3 Activation.International journal of molecular sciences · 2023Review
- Role of SIRT3 in neurological diseases and rehabilitation training.Metabolic brain disease · 2023Review
- Senescent melanocytes driven by glycolytic changes are characterized by melanosome transport dysfunction.Theranostics · 2023Article
- MiRNA-494 specifically inhibits SIRT3-mediated microglia activation in sepsis-associated encephalopathy.Translational cancer research · 2022Article
- Ubiquitin-specific protease 3 attenuates interleukin-1β-mediated chondrocyte senescence by deacetylating forkhead box O-3 via sirtuin-3.Bioengineered · 2022Article
- Nutrition Interventions of Herbal Compounds on Cellular Senescence.Oxidative medicine and cellular longevity · 2022Review
- Sirtuin 3 (SIRT3) Pathways in Age-Related Cardiovascular and Neurodegenerative Diseases.Biomedicines · 2021Review
- The metabolic roots of senescence: mechanisms and opportunities for intervention.Nature metabolism · 2021Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sirtuin 3 (SIRT3) is one of the seven mammalian sirtuins, which are homologs of the yeast Sir2 gene. SIRT3 is the only sirtuin reported to be associated with human life span. Many recent studies have indicated that SIRT3 levels are elevated by exercise and caloric restriction, but whether SIRT3 influences cell senescence under stressed conditions in human diploid fibroblasts has not been established. Our data showed that expression of SIRT3 is elevated in human diploid fibroblasts under low glucose (3.3 mM glucose) growth conditions and decreased under high glucose (25 mM glucose) growth conditions. We have demonstrated that SIRT3 interacts with forkhead box protein O1 (FOXO1). High glucose levels also increased aging phenotypes and FOXO1 acetylation level. We have demonstrated that overexpression of SIRT3 under high glucose conditions reduces FOXO1 acetylation, suggesting that deacetylation of FOXO1 by SIRT3 elevates the expression of the FOXO1 target genes, catalase, and manganese superoxide dismutase (MnSOD) while decreasing senescence phenotypes. We studied the effects of SIRT3 protein knockdown by shRNA under low glucose conditions. The data showed that shRNA-SIRT3 accelerated senescence phenotypes and acetylation of FOXO1; the expression level of catalase and MnSOD decreased compared with the control group. As a consequence, SIRT3 antagonized cellular senescence with the characteristic features of delayed SA-β-gal staining, senescence-associated heterochromatin foci (SAHF) formation, and p16(INK4A) expression. These results demonstrate for the first time that SIRT3 overexpression antagonizes high glucose-induced cellular senescence in human diploid fibroblasts via the SIRT3-FOXO1 signaling pathway.
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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.