ArticleNature metabolism2025
The pentose phosphate pathway controls oxidative protein folding and prevents ferroptosis in chondrocytes.
Article in Nature metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Biomimetic nanoparticles camouflaged with M2 macrophage membrane for osteoporosis therapy: A triple-action strategy that upregulates anti-inflammation and osteogenic responses while suppressing MMP-9.Materials today. Bio · 2026Article
- Ferroptosis as an approach to leverage cancer metabolism.Trends in cell biology · 2026Review
- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Regulating Glucose Metabolism Enzymes for Osteoporosis Therapy: Current and Future Approaches.International journal of molecular sciences · 2026Review
- Elucidating the Role of Oxidative Stress-Associated Genes FKBP Prolyl Isomerase 5 in Osteoarthritis Development and Immunological Milieu.Biological procedures online · 2026Article
- Immunometabolism, an emerging field in perioperative and critical care medicine: a narrative review.British journal of anaesthesia · 2026Review
- Reactive oxygen species (ROS) in cancer: from mechanism to therapeutic implications.Signal transduction and targeted therapy · 2026Review
- Comparative Phosphoproteomics of TwoJournal of fungi (Basel, Switzerland) · 2026Article
- Redox-metabolic circuits as a central regulator of T cell-based immunotherapy.Frontiers in immunology · 2026Review
- Dietary supplementation withFrontiers in microbiology · 2026Article
- Biomimetic dynamic nanomedicine SrHCF: Lattice self-reconstruction based on FeBioactive materials · 2026Article
- Targeting Metabolism in Cancer Therapy: Inhibitors and Approaches.Cancer treatment and research · 2026Review
- Hyperuricemia was associated with metabolic response against brain injury instead of metabolism syndrome in Tibet: a cross-sectional analysis.Frontiers in endocrinology · 2026Article
- A Nanomedicine Strategy: Spatiotemporally Programmed Delivery of Engineered Exosomes via Smart Scaffolds for Craniofacial Bone Regeneration.International journal of nanomedicine · 2026Review
- Review
- Ferroptosis and head and neck cancer: Mechanisms and therapeutic perspectives (Review).International journal of molecular medicine · 2025Review
- Multi-omics integration at cell type resolution uncovers gene-metabolite mechanisms underlying osteoarthritis heterogeneity.bioRxiv : the preprint server for biology · 2025Article
- Multidisciplinary analysis of the prognosis and biological function of NUBPL in gastric cancer.Frontiers in immunology · 2025Article
- Chondrocyte metabolic transition from proliferation to quiescence revealed by FLIM in postnatal mouse knee joints.Journal of tissue engineeringArticle
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Authors and funding
10 authors.
Funding
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Abstract
Bone lengthening and fracture repair depend on the anabolic properties of chondrocytes that function in an avascular milieu. The limited supply of oxygen and nutrients calls into question how biosynthesis and redox homeostasis are guaranteed. Here we show that glucose metabolism by the pentose phosphate pathway (PPP) is essential for endochondral ossification. Loss of glucose-6-phosphate dehydrogenase in chondrocytes does not affect cell proliferation because reversal of the non-oxidative PPP produces ribose-5-phosphate. However, the decreased NADPH production reduces glutathione recycling, resulting in decreased protection against the reactive oxygen species (ROS) produced during oxidative protein folding. The disturbed proteostasis activates the unfolded protein response and protein degradation. Moreover, the oxidative stress induces ferroptosis, which, together with altered matrix properties, results in a chondrodysplasia phenotype. Collectively, these data show that in hypoxia, the PPP is crucial to produce reducing power that confines ROS generated by oxidative protein folding and thereby controls proteostasis and prevents ferroptosis.
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