ArticleJCI insight2020
Accelerated osteocyte senescence and skeletal fragility in mice with type 2 diabetes.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.
- Effect of type 2 diabetes on biochemical markers of bone metabolism: a meta-analysis.Frontiers in physiology · 2024Pooled it
- Shared mechanisms of musculoskeletal dysfunction in type 2 diabetes mellitus: Insights into future therapeutic directions (Review).International journal of molecular medicine · 2026Review
- Cellular senescence and the SASP in skeletal ageing: convergent mechanisms of progressive bone loss in osteoporosis.Biogerontology · 2026Review
- DMP1-Cre expressing cells mediate the gain in bone mass and strength, but not the increase in bone remodeling, induced by ligands of the parathyroid hormone receptor.Bone research · 2026Article
- Diets Differently Affect Bone Health: Murine Models.International journal of molecular sciences · 2026Article
- Type 2 Diabetes Modulates Mesenchymal Stem Cell Response to Advanced Glycation End Products and N-Acetylcysteine Antioxidant Effect.Pharmaceutics · 2026Article
- Genetic and pharmacologic modulation of RAGE rescues the diabetes-mediated impairments to bone at multiple length scales.bioRxiv : the preprint server for biology · 2026Article
- Deconstructing senescence phenotypes in cells of the bone and bone marrow.The Journal of clinical investigation · 2026Article
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- Chronic low-grade inflammation drives skeletal aging and neurocognitive decline: inflammaging as a central hub coupling bone-brain aging.Frontiers in immunology · 2026Review
- Unveiling GDF-15: a new frontier in combating diabetic osteoporosis.Frontiers in medicine · 2026Review
- Immune-metabolic convergence in skeletal remodeling disorders: shared osteoimmune, senescent and lipid mechanisms across aging-related and immune-mediated bone disease.Frontiers in immunology · 2026Review
- NOX2-Driven Oxidative Stress Promotes EndMT and Uncouples Angiogenesis-Osteogenesis at the Bone-Implant Interface in Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Degenerating intervertebral discs in the streptozotocin-high-fat diet model of type 2 diabetes show extensive inflammation.Disease models & mechanisms · 2025Article
- New Aspects of the Pathophysiology of Diabetic Bone Fragility - Type 2 Diabetes Mellitus as a Disease of Accelerated Aging.Current osteoporosis reports · 2025Review
- Recent Advances in the Role of Osteocytes in Orthodontic Tooth Movement.International journal of molecular sciences · 2025Review
- The transcriptome and secreted factors of the intervertebral discs in STZ-HFD Type 2 diabetic male mice reveal extensive inflammation.bioRxiv : the preprint server for biology · 2025Article
- HydroWrap for T2DM-Related Fractures: A smart HBioactive materials · 2025Article
- The sex-specific effects of RAGE signaling and type 2 diabetes on mouse cortical bone mechanics, structure, and material properties.Mechanobiology in medicine · 2025Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
The worldwide prevalence of type 2 diabetes (T2D) is increasing. Despite normal to higher bone density, patients with T2D paradoxically have elevated fracture risk resulting, in part, from poor bone quality. Advanced glycation endproducts (AGEs) and inflammation as a consequence of enhanced receptor for AGE (RAGE) signaling are hypothesized culprits, although the exact mechanisms underlying skeletal dysfunction in T2D are unclear. Lack of inducible models that permit environmental (in obesity) and temporal (after skeletal maturity) control of T2D onset has hampered progress. Here, we show in C57BL/6 mice that a onetime pharmacological intervention (streptozotocin, STZ) initiated in adulthood combined with high-fat diet-induced (HFD-induced) obesity caused hallmark features of human adult-onset T2D, including prolonged hyperglycemia, insulin resistance, and pancreatic β cell dysfunction, but not complete destruction. In addition, HFD/STZ (i.e., T2D) resulted in several changes in bone quality that closely mirror those observed in humans, including compromised bone microarchitecture, reduced biomechanical strength, impaired bone material properties, altered bone turnover, and elevated levels of the AGE CML in bone and blood. Furthermore, T2D led to the premature accumulation of senescent osteocytes with a unique proinflammatory signature. These findings highlight the RAGE pathway and senescent cells as potential targets to treat diabetic 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 OpenQuestion graph.