ArticleScientific reports2023
SIRT6-PAI-1 axis is a promising therapeutic target in aging-related bone metabolic disruption.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- SERPINE1/PAI-1 in Skeletal Degeneration: A Proposed Context-Dependent Framework for Bone Remodeling Regulation.Calcified tissue international · 2026Review
- Review
- Accelerated biological aging: the role of chronic inflammation, weathering and novel therapeutic strategies.Frontiers in aging · 2026Review
- PAI-1: A Key Signal at the Crossroads of Stem Cell Differentiation and Senescence.International journal of molecular sciences · 2025Review
- Roles of plasminogen activator inhibitor-1 in aging-related muscle and bone loss in mice.Aging · 2025Article
- Epigenetic Regulation of Bone Healing: Implications for Fracture Repair and Clinical Treatment Strategies.The Yale journal of biology and medicine · 2025Review
- Sirt6 deficiency promotes senescence and age-associated intervertebral disc degeneration in mice.Bone research · 2025Article
- SIRT6 loss causes intervertebral disc degeneration in mice by promoting senescence and SASP status.bioRxiv : the preprint server for biology · 2024Article
- Effect and mechanism of curcumin on colon cancer cell senescence through early growth response 1 (EGR1).Translational cancer research · 2024Article
- Regulatory cellular and molecular networks in the bone microenvironment during aging.Life medicine · 2024Review
- A PAI-1 antagonist ameliorates hypophosphatemia in the Hyp vitamin D-resistant rickets model mouse.FEBS open bio · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanistic regulation of bone mass in aged animals is poorly understood. In this study, we examined the role of SIRT6, a longevity-associated factor, in osteocytes, using mice lacking Sirt6 in Dmp-1-expressing cells (cKO mice) and the MLO-Y4 osteocyte-like cell line. cKO mice exhibited increased osteocytic expression of Sost, Fgf23 and senescence inducing gene Pai-1 and the senescence markers p16 and Il-6, decreased serum phosphate levels, and low-turnover osteopenia. The cKO phenotype was reversed in mice that were a cross of PAI-1-null mice with cKO mice. Furthermore, senescence induction in MLO-Y4 cells increased the Fgf23 and Sost mRNA expression. Sirt6 knockout and senescence induction increased HIF-1α binding to the Fgf23 enhancer sequence. Bone mass and serum phosphate levels were higher in PAI-1-null aged mice than in wild-type mice. Therefore, SIRT6 agonists or PAI-1 inhibitors may be promising therapeutic options for aging-related bone metabolism disruptions.
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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.