ArticleJournal of orthopaedic translation2024
The senolytic agent ABT263 ameliorates osteoporosis caused by active vitamin D insufficiency through selective clearance of senescent skeletal cells.
Article in Journal of orthopaedic translation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Cellular senescence and the SASP in skeletal ageing: convergent mechanisms of progressive bone loss in osteoporosis.Biogerontology · 2026Review
- Bone aging: a paradigm of multiscale degeneration and targeted rejuvenation.Bone research · 2026Review
- Pathological Mechanism-Inspired Biomimetic Nano-Senotherapy for Reversing Experimental Atherosclerosis in ApoEAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Epigenetic Mechanisms of Vitamin D in the Aging Process: A Narrative Review.International journal of molecular sciences · 2026Review
- Targeting the FOXO4-p53 axis by retro-inverso peptide senolytic agents: a pharmacological strategy to mitigate brain aging and cognitive decline.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Zinc and metformin co-functionalized polyetheretherketone: A novel dental implant material tailored for the elderly.Journal of advanced research · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- A spatiotemporal atlas of senescence-associated secretory phenotype in fracture healing: stage-dependent mechanisms and therapeutic windows.Inflammation and regeneration · 2026Review
- Vitamin D deficiency and disease conditions relevant to: Orthopaedic translation.Journal of orthopaedic translation · 2026Review
- LncRNA HOXC-AS3 prevents chondrocyte senescence and osteoarthritis progression through miR-615-3p sponging and RRBP1 interaction.Cell & bioscience · 2026Article
- Senescence-associated secretory phenotype: the "pathogenic" factor driving orthopedic degenerative diseases and its regulation.Frontiers in aging · 2026Review
- From Neuron-Centric to Glia-Centric: How Aging Glial Networks Drive Neurodegenerative Disease.Journal of neurochemistry · 2026Review
- Biomaterials targeting senescent cells for bone regeneration: State-of-the-art and future perspectives.Bioactive materials · 2025Review
- Chk2 deletion rescues bone loss and cellular senescence induced by Bmi1 deficiency via regulation of Cyp1a1.Journal of orthopaedic translation · 2025Article
- New developments in osteoporosis, osteoarthritis and soft tissue repair.Journal of orthopaedic translation · 2024Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background/Objective: Active vitamin D insufficiency accelerates the development of osteoporosis, with senescent bone cells and the senescence-associated secretory phenotype (SASP) playing crucial roles. This study aimed to investigate whether the senolytic agent ABT263 could correct osteoporosis caused by active vitamin D insufficiency by selectively clearing senescent cells. Methods: Bone marrow mesenchymal stem cells (BM-MSCs) from young and aged mice were treated with ABT263 in vitro, and 1,25(OH) Results: ABT263 induced apoptosis in senescent BM-MSCs by downregulating Bcl2 and upregulating Bax expression. It also induced apoptosis in senescent BM-MSCs from 1,25(OH) Conclusion: ABT263 can correct osteoporosis caused by active vitamin D insufficiency by selectively clearing senescent skeletal cells, reducing oxidative stress, DNA damage, and SASP, and promoting bone formation while inhibiting bone resorption. These findings provide new insights into the potential therapeutic application of senolytic agents in the treatment of osteoporosis associated with active vitamin D insufficiency. The translational potential of this article: This study highlights the therapeutic potential of ABT263, a senolytic compound, in treating osteoporosis caused by active vitamin D insufficiency. By selectively eliminating senescent bone cells and their associated SASP, ABT263 intervention demonstrates the ability to restore bone homeostasis, prevent further bone loss, and promote bone formation. These findings contribute to the growing body of research supporting the use of senolytic therapies for the prevention and treatment of age-related bone disorders. The translational potential of this study lies in the development of novel therapeutic strategies targeting cellular senescence to combat osteoporosis, particularly in cases where vitamin D insufficiency is a contributing factor. Further clinical studies are warranted to validate the efficacy and safety of ABT263 and other senolytic agents in the treatment of osteoporosis in humans.
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