ReviewFrontiers in aging2026
Aging-related metabolic dysregulation in osteoporosis: mechanisms and therapeutic strategies.
Review in Frontiers in aging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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11 authors.
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Abstract
Purpose of review: This review aims to summarize recent advances in the mechanistic understanding of senile osteoporosis, with particular focus on the interconnected roles of cellular senescence, metabolic dysfunction, and systemic homeostatic imbalance in age-related skeletal degeneration. Recent findings: Emerging evidence indicates that senile osteoporosis is not driven solely by age-related hormonal decline, but by a complex network of biological processes involving senescence of bone marrow mesenchymal stem cells, accumulation of the senescence-associated secretory phenotype, mitochondrial dysfunction, oxidative stress, chronic low-grade inflammation, and disturbances in glucose and lipid metabolism. These alterations disrupt bone remodeling through key signaling pathways, including RANKL/OPG, Wnt/β-catenin, AMPK/SIRT1, NF-κB, and PI3K/Akt/mTOR. Together, these mechanisms impair osteogenesis, enhance osteoclastogenesis, deteriorate bone microarchitecture, and increase skeletal fragility. This broader pathophysiological framework may explain why conventional antiresorptive therapies, although effective in reducing bone resorption, often fail to fully restore the structural and functional deficits of the aging skeleton. Summary: Senile osteoporosis should be viewed as a systemic aging-related disorder involving both deterioration of the local bone microenvironment and whole-body metabolic dysregulation. Current evidence-based pharmacological treatments, including bisphosphonates, denosumab, teriparatide, abaloparatide, and romosozumab, remain central to fracture prevention and bone mass preservation. However, these interventions do not fully reverse the biological processes of skeletal aging. Emerging strategies targeting cellular senescence, the senescence-associated secretory phenotype, mitochondrial dysfunction, oxidative stress, nutrient-sensing pathways, and gut microbiota are under active investigation and may complement established therapies in the future. A clearer distinction between approved anti-osteoporotic drugs and experimental geroscience-based interventions is essential for translating mechanistic insights into clinically meaningful treatment strategies.
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