ArticleNature communications2025
Regulation of enzymatic lipid peroxidation in osteoblasts protects against postmenopausal osteoporosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Oxidized-Lipid Signaling and Ferroptosis as Downstream Mechanisms of Titanium-Associated Peri-Implant Bone Loss.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Surface Modification of Titanium with EGCG and Hexamethylenediamine Coating for BMP‑2 Grafting: An Investigation of Osteogenic Properties.ACS omega · 2026Article
- Tri-modal nanocatalytic microenvironment regulations for macrophage reprogramming and osteoporotic fracture healing promotion.Materials today. Bio · 2026Article
- Integration of metabolomics and machine learning algorithm for discovery of early diagnostic biomarkers of osteoporosis.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Estrogen deficiency as a common driver and integrative mechanism in osteoporosis‑osteoarthritis comorbidity (Review).Molecular medicine reports · 2026Review
- Fatty acid uptake mediated by FABP4 promotes the formation of CD8Oncogenesis · 2026Article
- Yishen Gushu formula exerts osteoprotective effects in OVX-Induced PMOP rats: role of ferroptosis Inhibition and iron metabolism correction.Hereditas · 2026Article
- Strontium-baicalein coated β-tricalcium phosphate scaffold enhances diabetic bone regeneration via synergistic ROS scavenging and osteogenic activation.Regenerative biomaterials · 2026Article
- Global, Regional, and National Sex Disparities in the Burden of Malignant Neoplasms of Bone and Articular Cartilage: a Systematic Analysis and Projections to 2050.Annals of surgical oncology · 2026Article
- The estrogen-ferroptosis axis in postmenopausal osteoporosis, osteoarthritis, and intervertebral disc degeneration: shared mechanisms and emerging evidence.Frontiers in immunology · 2026Review
- A Review of the Mechanisms, Biological Basis, and Active Ingredients of Traditional Chinese Medicine Formulations in Regulating Organ Function to Alleviate Osteoporosis.Endocrine, metabolic & immune disorders drug targets · 2026Review
- A pH-Responsive Polysaccharide Hydrogel Modulates Oxygen Delivery and Immunometabolic Remodeling for Diabetic Bone Regeneration.Research (Washington, D.C.) · 2026Article
- Estrogen promotes the angiogenesis and osteogenesis of bone marrow stromal cells via regulating ESR1/RUNX2 axis.Food & nutrition research · 2026Article
- Oxidative stress and bone marrow adipocytes: Molecular mechanisms and possible implications.Journal of orthopaedic translation · 2026Review
- The interplay of estrogen, gut microbiome, and bone immunity in osteoporosis.Cell communication and signaling : CCS · 2025Review
- Advancement in smart bone implants: the latest multifunctional strategies and synergistic mechanisms for tissue repair and regeneration.Bioactive materials · 2025Review
- Oxidative Stress and Biomarkers in Craniofacial Fractures Healing: From Lipid Peroxidation to Antioxidant Therapies.Antioxidants (Basel, Switzerland) · 2025Review
- New Perspectives on Postmenopausal Osteoporosis: Mechanisms and Potential Therapeutic Strategies of Sirtuins and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Review
- ACT001 improves OVX-induced osteoporosis by suppressing the NF-κB/NLRP3 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
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Authors and funding
21 authors.
Funding
Abstract
Oxidative stress plays a critical role in postmenopausal osteoporosis, yet its impact on osteoblasts remains underexplored, limiting therapeutic advances. Our study identifies phospholipid peroxidation in osteoblasts as a key feature of postmenopausal osteoporosis. Estrogen regulates the transcription of glutathione peroxidase 4 (GPX4), an enzyme crucial for reducing phospholipid peroxides in osteoblasts. The deficiency of estrogen reduces GPX4 expression and increases phospholipid peroxidation in osteoblasts. Inhibition or knockout of GPX4 impairs osteoblastogenesis, while the elimination of phospholipid peroxides rescues bone formation and mitigates osteoporosis. Mechanistically, 4-hydroxynonenal, an end-product of phospholipid peroxidation, binds to integrin-linked kinase and triggers its protein degradation, disrupting RUNX2 signaling and inhibiting osteoblastogenesis. Importantly, we identified two natural allosteric activators of GPX4, 6- and 8-Gingerols, which promote osteoblastogenesis and demonstrate anti-osteoporotic effects. Our findings highlight the detrimental role of phospholipid peroxidation in osteoblastogenesis and underscore GPX4 as a promising therapeutic target for osteoporosis treatment.
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