ReviewCellular and molecular life sciences : CMLS2015
Osteoblast dysfunctions in bone diseases: from cellular and molecular mechanisms to therapeutic strategies.
Review in Cellular and molecular life sciences : CMLS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
52 citing papers in PubMed, 82 citations in OpenAlex.
- Article
- Multi-omics and causal inference reveal lactylation-based osteoblast regulatory networks and drug candidates.iScience · 2026Article
- MicroRNA network regulation of developmental bone toxicity in a human embryonic stem cell osteogenic model.NAM journal · 2026Article
- Free amino acid-rich egg yolk protein hydrolysate promotes osteogenesis of MC3T3-E1 cells association withFrontiers in nutrition · 2026Article
- Role of mesenchymal stem cell-derived exosomal non-coding RNAs in bone and bone-related disorders.World journal of stem cells · 2025Review
- Narirutin mitigates inflammatory arthritis and osteoporosis through modulating macrophage phenotype and osteoclastogenesis.Journal of orthopaedic translation · 2025Article
- Subchondral injection of human umbilical cord mesenchymal stem cells ameliorates knee osteoarthritis by inhibiting osteoblast apoptosis and TGF-beta activity.Stem cell research & therapy · 2025Article
- Jingui Shenqi Wan alleviates bone loss induced by primary osteoporosis by inhibiting osteoblast pyroptosis.Journal of orthopaedic surgery and research · 2025Article
- Investigation of Oxidative-Stress Impact on Human Osteoblasts During Orthodontic Tooth Movement Using an In Vitro Tension Model.International journal of molecular sciences · 2024Article
- Eucommia ulmoides Oliver polysaccharide alleviates glucocorticoid-induced osteoporosis by stimulating bone formation via ERK/BMP-2/SMAD signaling.Scientific reports · 2024Article
- HIV Modulates Osteoblast Differentiation via Upregulation of RANKL and Vitronectin.Pathogens (Basel, Switzerland) · 2024Article
- USP36 regulates the proliferation, survival, and differentiation of hFOB1.19 osteoblast.Journal of orthopaedic surgery and research · 2024Article
- The Mohawk homeobox gene represents a marker and osteo-inhibitory factor in calvarial suture osteoprogenitor cells.Cell death & disease · 2024Article
- METTL3-mediated m6A modification increases Hspa1a stability to inhibit osteoblast aging.Cell death discovery · 2024Article
- In Vitro Modelling of Osteogenesis Imperfecta with Patient-Derived Induced Mesenchymal Stem Cells.International journal of molecular sciences · 2024Article
- Article
- Article
- Osteogenic Activities of Trifolirhizin as a Bioactive Compound for the Differentiation of Osteogenic Cells.International journal of molecular sciences · 2023Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several metabolic, genetic and oncogenic bone diseases are characterized by defective or excessive bone formation. These abnormalities are caused by dysfunctions in the commitment, differentiation or survival of cells of the osteoblast lineage. During the recent years, significant advances have been made in our understanding of the cellular and molecular mechanisms underlying the osteoblast dysfunctions in osteoporosis, skeletal dysplasias and primary bone tumors. This led to suggest novel therapeutic approaches to correct these abnormalities such as the modulation of WNT signaling, the pharmacological modulation of proteasome-mediated protein degradation, the induction of osteoprogenitor cell differentiation, the repression of cancer cell proliferation and the manipulation of epigenetic mechanisms. This article reviews our current understanding of the major cellular and molecular mechanisms inducing osteoblastic cell abnormalities in age-related bone loss, genetic skeletal dysplasias and primary bone tumors, and discusses emerging therapeutic strategies to counteract the osteoblast abnormalities in these disorders of bone formation.
Indexed as
Identifiers
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.