ReviewSeminars in hematology2012
Proteasome inhibitors and bone disease.
Review in Seminars in hematology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Complement C3a promotes the formation of osteoclasts by inhibiting Sirt1 to activate the PI3K/PDK1/SGK3 pathway in patients with multiple myeloma.Journal of translational medicine · 2025Article
- An overview of multiple myeloma: A monoclonal plasma cell malignancy's diagnosis, management, and treatment modalities.Saudi journal of biological sciences · 2024Review
- Dynamics of Bone Disease Biomarkers Dickkopf-1 and Sclerostin in Patients with Multiple Myeloma.Journal of clinical medicine · 2023Article
- Pathogenesis and Treatment of Myeloma-Related Bone Disease.International journal of molecular sciences · 2022Review
- Proteasome inhibition-enhanced fracture repair is associated with increased mesenchymal progenitor cells in mice.PloS one · 2022Article
- Expression and Role of Ubiquitin-Specific Peptidases in Osteoblasts.International journal of molecular sciences · 2021Review
- Article
- Additive Benefits of Radium-223 Dichloride and Bortezomib Combination in a Systemic Multiple Myeloma Mouse Model.International journal of molecular sciences · 2021Article
- Fractions of Shen-Sui-Tong-Zhi Formula Enhance OsteogenesisFrontiers in pharmacology · 2021Article
- Effect of bortezomib on proliferation and apoptosis of myeloma cells by activating Wnt/β-catenin signaling pathway.Oncology letters · 2020Article
- Increased PLEKHO1 within osteoblasts suppresses Smad-dependent BMP signaling to inhibit bone formation during aging.Aging cell · 2017Article
- Update on the optimal use of bortezomib in the treatment of multiple myeloma.Cancer management and research · 2017Review
- E11/Podoplanin Protein Stabilization Through Inhibition of the Proteasome Promotes Osteocyte Differentiation in Murine in Vitro Models.Journal of cellular physiology · 2016Article
- Review
- Bortezomib modulates CHIT1 and YKL40 in monocyte-derived osteoclast and in myeloma cells.Frontiers in pharmacology · 2015Article
- Mesenchymal stem cell contact promotes CCN1 splicing and transcription in myeloma cells.Cell communication and signaling : CCS · 2014Article
- Increased serum levels of MIP-1alpha correlate with bone disease and angiogenic cytokines in patients with multiple myeloma.Medical oncology (Northwood, London, England) · 2014Article
- Dickkopf-1 is a key regulator of myeloma bone disease: opportunities and challenges for therapeutic intervention.Blood reviews · 2013Review
- Characterization of the molecular mechanism of the bone-anabolic activity of carfilzomib in multiple myeloma.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Bone disease in patients with multiple myeloma (MM) is characterized by increase in the numbers and activity of bone-resorpting osteoclasts and decrease in the number and function of bone-formation osteoblasts. MM-triggered inhibition of bone formation may stem from suppression of Wnt/β-catenin signaling, a pivotal pathway in the differentiation of mesenchymal stem cells (MSC) into osteoblasts, and regulating production of receptor activator of nuclear factor-κB ligand (RANKL)/osteoprotegerin (OPG) axis by osteoblasts. Proteasome inhibitors (PIs), such as bortezomib (Bz), induce activation of Wnt/β-catenin pathway and MSC differentiation toward osteoblasts. PIs also suppress osteoclastogenesis, possibly through regulating multiple pathways including NF-κB, Bim, and the ratio of RANKL/OPG. The critical role of PI in increasing osteoblast function and suppression of osteoclast activity is highlighted by clinical evidence of increases in bone formation and decreases in bone resorption makers. This review will discuss the function of PIs in stimulating bone formation and suppression of bone resorption, and the mechanism underlying this process that leads to inhibition bone disease in MM patients.
Indexed as
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What OpenQuestion holds
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.