ReviewBiomedicines2025
Beyond Bone Loss: A Biology Perspective on Osteoporosis Pathogenesis, Multi-Omics Approaches, and Interconnected Mechanisms.
Review in Biomedicines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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
17 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Pharmacological effects ofFrontiers in pharmacology · 2026Pooled it
- CircRNAs as biomarkers for osteoporosis: a systematic review and meta-analysis.Frontiers in endocrinology · 2026Pooled it
- Epigenetic Regulation of Bone Homeostasis in Osteoporosis: Mechanisms, Evidence Gaps, and Translational Prospects.Cell biochemistry and function · 2026Review
- Article
- Causal genes for osteoporosis: Mendelian randomization analysis with multilayer xQTL data.Medicine · 2026Article
- A Novel SIRT1 Activator Hydroxygenkwanin Alleviates Osteoporosis by Inhibiting Ferroptosis and Lactylation in Skeletal Stem/Progenitor Cells.Antioxidants (Basel, Switzerland) · 2026Article
- FeBioengineering (Basel, Switzerland) · 2026Article
- Osteoporosis and Chronic Inflammation: A Global Bibliometric Analysis Between 1994 and 2025.International journal of rheumatic diseases · 2026Article
- Serum Dkk-1 Is Associated with Pain Intensity, Flare-Ups, and Bone Mineral Density in Non-Obese Patients with Knee Osteoarthritis: A Single-Center, Cross-Sectional Study.International journal of molecular sciences · 2026Article
- Aging-related metabolic dysregulation in osteoporosis: mechanisms and therapeutic strategies.Frontiers in aging · 2026Review
- Clinically constrained Bayesian network analysis of immune-metabolic factors associated with bone mineral density in a real-world orthopedic cohort.Frontiers in surgery · 2026Article
- The role and mechanisms of bone microenvironment regulators in osteoporosis: novel intervention strategies for addressing the challenges of aging.Frontiers in endocrinology · 2026Review
- Comprehensive profiling of gut microbiota in postmenopausal osteoporosis.Turkish journal of medical sciences · 2026Article
- Phenolic-derived compounds in osteoporosis-Mechanisms, clinical evidence, and drug delivery: A review.Biomolecules & biomedicine · 2025Review
- Construction and validation of a multi-dimensional health indicator-driven osteoporosis risk prediction model: a large-sample cross-sectional study based on two centers.BMC musculoskeletal disorders · 2025Article
- Article
- DNA methylation and immune regulation in osteoporosis: emerging epigenetic targets for drug discovery.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Osteoporosis is a systemic bone disorder characterized by decreased bone mass and deteriorated microarchitecture, leading to an increased risk of fractures. Recent studies have revealed that its pathogenesis involves complex biological processes beyond bone remodeling, including oxidative stress, chronic inflammation, cellular senescence, osteoimmunology, gut microbiota alterations, and epigenetic modifications. Oxidative stress disrupts bone homeostasis by promoting excessive free radical production and osteoclast activity. Chronic inflammation and the accumulation of senescent cells impair skeletal repair mechanisms. Advances in osteoimmunology have highlighted the critical role of immune-bone crosstalk in regulating bone resorption and formation. Moreover, the gut-bone axis, mediated by microbial metabolites, influences bone metabolism through immune and endocrine pathways. Epigenetic changes, such as DNA methylation and histone modification, contribute to gene-environment interactions, affecting disease progression. Multi-omics approaches (genomics, proteomics, and metabolomics) systematically identify molecular networks and comorbid links with diabetes/cardiovascular diseases, revealing pathological feedback loops that exacerbate bone loss. In conclusion, osteoporosis pathogenesis extends beyond bone remodeling to encompass systemic inflammation, immunometabolic dysregulation, and gut microbiota-host interactions. Future research should focus on integrating multi-omics biomarkers with targeted therapies to advance precision medicine strategies for osteoporosis prevention and treatment.
Indexed as
Identifiers
What Socratic 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 Socratic graph.