ArticleScientific reports2015
Overexpression of Sirtuin 6 suppresses cellular senescence and NF-κB mediated inflammatory responses in osteoarthritis development.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Meta-analysis Integrated With Multi-omics Data Analysis to Elucidate Pathogenic Mechanisms of Age-Related Knee Osteoarthritis in Mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Pooled it
- Critical role of Sirtuin 6 (SIRT6) in osteoarthritis chondrocytes: the interaction among various biological processes.Annals of medicine · 2026Review
- SIRT6 activator MDL-800 alleviates periodontal inflammation by inhibiting AIM2 pathway.Acta pharmaceutica Sinica. B · 2026Article
- The Influence of Sirtuin 6 on Chondrocyte Senescence in Osteoarthritis Under Aging: Focusing on Mitochondrial Dysfunction and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Review
- Alleviating the IL-1β-stimulated extracellular matrix degradation in osteoarthritis, and chondrocyte inflammation byBiomolecules & biomedicine · 2025Article
- Novel perspectives on leptin in osteoarthritis: Focus on aging.Genes & diseases · 2024Review
- Serum Sirt6 as a Potential Biomarker for Osteoarthritis and its Correlation with IL-6 Alterations.Indian journal of orthopaedics · 2024Article
- Cellular Senescence: The Driving Force of Musculoskeletal Diseases.Biomedicines · 2024Review
- Research advances on silence information regulator 6 as a potential therapeutic target for bone regeneration and repair.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Review
- Skeletal phenotypes and molecular mechanisms in aging mice.Zoological research · 2024Review
- Hepatic Sirt6 activation abrogates acute liver failure.Cell death & disease · 2024Article
- Single‑cell sequencing, genetics, and epigenetics reveal mesenchymal stem cell senescence in osteoarthritis (Review).International journal of molecular medicine · 2024Review
- Sirt6 promotes DNA damage repair in osteoarthritis chondrocytes by activating the Keap1/Nrf2/HO-1 signaling pathway.Cell cycle (Georgetown, Tex.) · 2024Article
- Advanced Progress of Histone Deacetylases in Rheumatic Diseases.Journal of inflammation research · 2024Review
- Sirtuin 6 activation rescues the age-related decline in DNA damage repair in primary human chondrocytes.Aging · 2023Article
- Role and molecular mechanism of ghrelin in degenerative musculoskeletal disorders.Journal of cellular and molecular medicine · 2023Review
- Cartilage-specificAnnals of the rheumatic diseases · 2023Article
- Oxidative stress as a key modulator of cell fate decision in osteoarthritis and osteoporosis: a narrative review.Cellular & molecular biology letters · 2023Review
- Article
- Modulation of SIRT6 activity acts as an emerging therapeutic implication for pathological disorders in the skeletal system.Genes & diseases · 2023Review
21 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of our study was to evaluate if Sirt6, a NAD + dependent histone deacetylase, plays a protective role in cartilage degeneration by suppressing cellular senescence and inflammatory responses. The expression level of sirt6 in normal and OA human knee articular cartilage was compared by immunofluorescence and western blotting. The effect of sirt6 overexpression on replicative senescence of chondrocytes and NF-κB target genes expression was evaluated. Histological assessment of OA mice knee joint was carried out to assess the in vivo effects of sirt6 overexpression on mice chondrocytes. We found sirt6 level was significantly decreased in the articular chondrocytes of OA patients compare to normal human. SA-β-gal staining revealed that overexpression of sirt6 suppressed replicative senescence of chondrocytes. Meanwhile, the expression of NF-κB dependent genes were significantly attenuated by sirt6 overxpression. Safranin-O staining and OARSI score of knee joint cartilage in OA mice revealed that Lenti-Sirt6 intraarticular injection could protect mice chondrocytes from degeneration. These data strongly suggest that overexpression of Sirt6 can prevent OA development by reducing both the inflammatory response and chondrocytes senescence. Therefore, the development of specific activators of Sirt6 may have therapeutic potential for the treatment of OA.
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