ArticleBone research2022
Targeting ferroptosis suppresses osteocyte glucolipotoxicity and alleviates diabetic osteoporosis.
Article in Bone research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.
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Who cites it
154 citing papers in PubMed, 1 synthesis or guideline pooled it, 228 citations in OpenAlex.
- The role of ferroptosis in osteoporosis: a cellular perspective on osteoblast, osteoclast and osteocyte dysfunction.Frontiers in endocrinology · 2026Pooled it
- Effect of rhPTH(1-34) and alendronate on the treatment of type 2 diabetic bone disease.Frontiers in endocrinology · 2025Trial
- A universal consuming endogenous HBioactive materials · 2027Article
- The miR-212-3p/transferrin axis promotes bone regeneration by modulating iron homeostasis through Schwann cell Exosome-BMSCs communication.Bioactive materials · 2026Article
- Cell Type-Specific Ferroptosis Regulatory Networks in the Bone Microenvironment: Implications for the Pathogenesis and Treatment of Osteoporosis.Traffic (Copenhagen, Denmark) · 2026Review
- Ferroptosis in skeletal muscle: from molecular mechanisms to therapeutic interventions.Journal of orthopaedic translation · 2026Review
- Aerobic Exercise Mitigates Experimental Knee Osteoarthritis via Inhibition of cGAS-STING Signaling.Microbiology and immunology · 2026Article
- Insights into taurine therapy for periodontitis: Targeting osteocyte ferroptosis to mitigate obesity-exacerbated bone damage.Redox biology · 2026Article
- Heme Oxygenase-1 in Bone Remodeling: Molecular Mechanisms and Therapeutic Implications.Biomolecules · 2026Review
- Orchestrated Engineered Polyphenol-Peptide Condensates Coupled With β-GP Reverses Diabetic Osteoporosis by Remodeling Mitophagy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Bioinformatics-based identification of ferroptosis-related biomarkers and immune infiltration in retinoblastoma.Translational cancer research · 2026Article
- Curcumin Alleviates the Osteogenesis Inhibition and the Aging Process in BMSCs Induced by Iron Overload Through Activating the NRF2/GPX4 Pathway.Phytotherapy research : PTR · 2026Article
- Huashi Baidu formula may attenuate adriamycin-induced myocardial injury via modulating NRF2-ATF3-SRXN1 axis-mediated ferroptosis.Chinese herbal medicines · 2026Article
- Closed-loop iron chelate recycling via molecularly imprinted hydrogels suppresses ferroptosis.Nature communications · 2026Article
- Milk-derived exosome-based strategy targeting ferroptosis-glycolysis network promotes bone regeneration in diabetic aging comorbidity.Journal of nanobiotechnology · 2026Article
- Beyond M1/M2: The Pivotal Role of Macrophage Metabolic Reprogramming in Chronic Bone Disease and Targeted Intervention.International journal of molecular sciences · 2026Review
- CD73Nature communications · 2026Article
- Targeting Ferroptosis With Natural Products for the Treatment of Skeletal System Disease: An Updated Review.Journal of cellular and molecular medicine · 2026Review
- Spectrum and functions of ion channels and transporters in osteoclasts.Bone research · 2026Review
- MYO1C is a urinary extracellular vesicle biomarker and mediator of podocyte injury in diabetic nephropathy.JCI insight · 2026Article
94 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetic osteoporosis (DOP) is the leading complication continuously threatening the bone health of patients with diabetes. A key pathogenic factor in DOP is loss of osteocyte viability. However, the mechanism of osteocyte death remains unclear. Here, we identified ferroptosis, which is iron-dependent programmed cell death, as a critical mechanism of osteocyte death in murine models of DOP. The diabetic microenvironment significantly enhanced osteocyte ferroptosis in vitro, as shown by the substantial lipid peroxidation, iron overload, and aberrant activation of the ferroptosis pathway. RNA sequencing showed that heme oxygenase-1 (HO-1) expression was notably upregulated in ferroptotic osteocytes. Further findings revealed that HO-1 was essential for osteocyte ferroptosis in DOP and that its promoter activity was controlled by the interaction between the upstream NRF2 and c-JUN transcription factors. Targeting ferroptosis or HO-1 efficiently rescued osteocyte death in DOP by disrupting the vicious cycle between lipid peroxidation and HO-1 activation, eventually ameliorating trabecular deterioration. Our study provides insight into DOP pathogenesis, and our results provide a mechanism-based strategy for clinical DOP treatment.
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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.