ReviewWorld journal of diabetes2025
Diabetic bone fragility through advanced glycation end product-collagen axis: Mechanisms and therapy of sodium glucose cotransporter 2 inhibitors.
Review in World journal of diabetes, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed.
- HALP score-adjusted FRAXplus tool effectively predicts hip fracture risk in elderly women with type 2 diabetes mellitus.BMC endocrine disorders · 2026Article
- Long-term trajectories and cumulative exposure of the triglyceride-glucose-frailty index in relation to hip fracture risk: evidence from a large-scale population-based cohort.Archives of osteoporosis · 2026Article
- Combined impact of glucose variability and mineral disorders on mortality and severe cardiorenal events in critically ill CKD patients: a multicenter cohort study.Frontiers in medicine · 2026Article
- Romosozumab Efficacy in Osteoporosis: Influence of Diabetes and Previous Antiresorptive Therapy: A Single Centre Experience.Clinical medicine insights. Endocrinology and diabetes · 2026Article
- Diabetes-Related Metabolic Osteoarthritis: Advanced Glycation-Collagen Axis, Cartilage Stiffening, and Biomaterials-Based Therapeutic Strategies.International journal of nanomedicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
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Abstract
Type 2 diabetes markedly elevates fracture risk despite normal or high bone mineral density, a paradox reflecting qualitative skeletal deficits rather than loss of mass. Chronic hyperglycemia fosters the accumulation of advanced glycation end products in bone; their nonenzymatic crosslinks stiffen type I collagen, impair mineralization, and erode mechanical strength. By engaging the receptor for advanced glycation end products, these adducts activate nuclear factorκB and mitogen-activated protein kinase cascades, amplifying oxidative stress, inflammation, osteoblast dysfunction, and osteoclastogenesis. This review synthesizes epidemiological data from type 1 and type 2 diabetes, highlights the limits of densitybased skeletal assessment, and details the molecular pathology of the glycation-collagen axis. It also appraises antiglycation therapies, including formation inhibitors, crosslink breakers and receptor antagonists, with a particular focus on sodium-glucose cotransporter 2 inhibitors that couple glycemic control with modulation of the glycation pathway. By integrating recent basic and clinical advances, we propose a mechanistic framework for diabetic bone disease and outline strategies to mitigate glycationdriven skeletal fragility.
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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.