ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018
Proteasome inhibitor bortezomib is a novel therapeutic agent for focal radiation-induced osteoporosis.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
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- Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure.JBMR plus · 2025Article
- Insights into age-related osteoporosis from senescence-based preclinical models and human accelerated aging paradigms.Mechanisms of ageing and development · 2025Review
- Effects of ADRM1 on osteoblast differentiation and mineralization in osteoporosis.American journal of translational research · 2025Article
- An updated overview of the search for biomarkers of osteoporosis based on human proteomics.Journal of orthopaedic translation · 2024Review
- Targeting CDC42 reduces skeletal degeneration after hematopoietic stem cell transplantation.Blood advances · 2024Article
- Therapeutic potential of carbon dots fromAnnals of translational medicine · 2024Article
- Small-molecule amines: a big role in the regulation of bone homeostasis.Bone research · 2023Review
- Bone Marrow Adiposity in Models of Radiation- and Aging-Related Bone Loss Is Dependent on Cellular Senescence.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Targeted clearance of p21- but not p16-positive senescent cells prevents radiation-induced osteoporosis and increased marrow adiposity.Aging cell · 2022Article
- Ionizing Radiation Activates Mitochondrial Function in Osteoclasts and Causes Bone Loss in Young Adult Male Mice.International journal of molecular sciences · 2022Article
- The pathophysiology of osteoporosis in obesity and type 2 diabetes in aging women and men: The mechanisms and roles of increased bone marrow adiposity.Frontiers in endocrinology · 2022Review
- Bone Aging, Cellular Senescence, and Osteoporosis.JBMR plus · 2021Review
- Skeletal Aging and Osteoporosis: Mechanisms and Therapeutics.International journal of molecular sciences · 2021Review
- Inhibition of the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) stimulates osteoblastogenesis by potentiating bone morphogenetic protein 2 (BMP2) responses.Journal of cellular physiology · 2021Article
- ULK1 Suppresses Osteoclast Differentiation and Bone Resorption via Inhibiting Syk-JNK through DOK3.Oxidative medicine and cellular longevity · 2021Article
- Targeted Reduction of Senescent Cell Burden Alleviates Focal Radiotherapy-Related Bone Loss.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- Systematic Pharmacological Methodology to Explore the Pharmacological Mechanism of Siwu Decoction for Osteoporosis.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- The emerging role of IMD 0354 on bone homeostasis by suppressing osteoclastogenesis and bone resorption, but without affecting bone formation.Cell death & disease · 2019Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Bone atrophy and its related fragility fractures are frequent, late side effects of radiotherapy in cancer survivors and have a detrimental impact on their quality of life. In another study, we showed that parathyroid hormone 1-34 and anti-sclerostin antibody attenuates radiation-induced bone damage by accelerating DNA repair in osteoblasts. DNA damage responses are partially regulated by the ubiquitin proteasome pathway. In the current study, we examined whether proteasome inhibitors have similar bone-protective effects against radiation damage. MG132 treatment greatly reduced radiation-induced apoptosis in cultured osteoblastic cells. This survival effect was owing to accelerated DNA repair as revealed by γH2AX foci and comet assays and to the up-regulation of Ku70 and DNA-dependent protein kinase, catalytic subunit, essential DNA repair proteins in the nonhomologous end-joining pathway. Administration of bortezomib (Bzb) reversed the loss of trabecular bone structure and strength in mice at 4 wk after focal radiation. Histomorphometry revealed that Bzb significantly increased the number of osteoblasts and activity in the irradiated area and suppressed the number and activity of osteoclasts, regardless of irradiation. Two weeks of Bzb treatment accelerated DNA repair in bone-lining osteoblasts and thus promoted their survival. Meanwhile, it also inhibited bone marrow adiposity. Taken together, we demonstrate a novel role of proteasome inhibitors in treating radiation-induced osteoporosis.-Chandra, A., Wang, L., Young, T., Zhong, L., Tseng, W.-J., Levine, M. A., Cengel, K., Liu, X. S., Zhang, Y., Pignolo, R. J., Qin, L. Proteasome inhibitor bortezomib is a novel therapeutic agent for focal radiation-induced osteoporosis.
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