ArticleScientific reports2024
Moderate mechanical stress suppresses chondrocyte ferroptosis in osteoarthritis by regulating NF-κB p65/GPX4 signaling pathway.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Histological and Immunohistochemical Methods in Normal and Osteoarthritic Knee Cartilage of Rat and Rabbit Models: A Literature Review.International journal of molecular sciences · 2025Pooled it
- Signal-driven interplay between lipid peroxidation and ferroptosis orchestrates osteoarthritis degeneration.Journal of orthopaedic translation · 2026Review
- Aerobic Exercise-Mediated Regulation of Ferroptosis in Skeletal Disorders: Molecular Mechanisms and Potential Applications.Biomolecules · 2026Review
- Exercise therapy-associated changes in Periostin (POSTN) osteoarthritis are linked to Hippo-YAP signaling.Molecular biology reports · 2026Article
- The role of exercise in MFN2 regulation in osteoarthritis.Molecular biology reports · 2026Review
- Linoleic acid accelerates osteoarthritis progression in male rats by targeting iron-sulfur clusters to drive ferroptosis in chondrocytes.Nature communications · 2026Article
- Metabolic Mechanisms of Hexavalent Chromium-Induced Splenic Immune Injury via Oxidative Stress and Ferroptosis Pathways in New Zealand Rabbits.Metabolites · 2026Article
- Closed-loop iron chelate recycling via molecularly imprinted hydrogels suppresses ferroptosis.Nature communications · 2026Article
- Exploring mitochondrial functions and dysfunctions in chondrocytes: toward the identification of novel therapies for osteoarthritis.Bone research · 2026Review
- Heat stress induces ferroptosis in intramuscular preadipocytes of Hu sheep via activation of the TNF-α/NF-κB/GPX4 signaling axis.Food chemistry. Molecular sciences · 2026Article
- Metabolic pathways and cell death modalities in diabetic complications: unraveling pyroptosis, ferroptosis, cuproptosis, and disulfidptosis.Cell death discovery · 2026Review
- Targeting Ferroptosis With Natural Products for the Treatment of Skeletal System Disease: An Updated Review.Journal of cellular and molecular medicine · 2026Review
- Long-term mechanical loading aggravates osteoarthritis through a pro-apoptotic inflammatory microenvironment.Journal of biomedical research · 2026Article
- Sertad1 exacerbates cardiomyocytes ferroptosis in sepsis-induced myocardial injury by inhibiting HIPK2.Molecular biology reports · 2026Article
- Effects of Mechanical Stress on Bone and Cartilage Metabolism: How Mechanical Stress Affects Energy Metabolism in Bone and Cartilage Tissues (Our Research Overview): Mini Review.International journal of molecular sciences · 2026Review
- LOXL1, THY1, and TYMS define an annotation-derived hemoglobin-associated immunotranscriptomic signature in osteoarthritis cartilage.Frontiers in immunology · 2026Article
- The estrogen-ferroptosis axis in postmenopausal osteoporosis, osteoarthritis, and intervertebral disc degeneration: shared mechanisms and emerging evidence.Frontiers in immunology · 2026Review
- Research progress on the mechanism of chondrocyte ferroptosis in osteoarthritis.Frontiers in immunology · 2026Review
- NF-κB signaling in osteoarthritis: integrating mechanical stress, innate immunity, and cartilage degeneration.Frontiers in immunology · 2026Review
- Potential crosstalk between ferroptosis and immunosenescence in osteoarthritis: evidence integration and translational insights from the osteoimmune microenvironment.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Ferroptosis is a recently identified form of programmed cell death that plays an important role in the pathophysiological process of osteoarthritis (OA). Herein, we investigated the protective effect of moderate mechanical stress on chondrocyte ferroptosis and further revealed the internal molecular mechanism. Intra-articular injection of sodium iodoacetate (MIA) was conducted to induce the rat model of OA in vivo, meanwhile, interleukin-1 beta (IL-1β) was treated to chondrocytes to induce the OA cell model in vitro. The OA phenotype was analyzed by histology and microcomputed tomography, the ferroptosis was analyzed by transmission electron microscope and immunofluorescence. The expression of ferroptosis and cartilage metabolism-related factors was analyzed by immunohistochemical and Western blot. Animal experiments revealed that moderate-intensity treadmill exercise could effectively reduce chondrocyte ferroptosis and cartilage matrix degradation in MIA-induced OA rats. Cell experiments showed that 4-h cyclic tensile strain intervention could activate Nrf2 and inhibit the NF-κB signaling pathway, increase the expression of Col2a1, GPX4, and SLC7A11, decrease the expression of MMP13 and P53, thereby restraining IL-1β-induced chondrocyte ferroptosis and degeneration. Inhibition of NF-κB signaling pathway relieved the chondrocyte ferroptosis and degeneration. Meanwhile, overexpression of NF-κB by recombinant lentivirus reversed the positive effect of CTS on chondrocytes. Moderate mechanical stress could activate the Nrf2 antioxidant system, inhibit the NF-κB p65 signaling pathway, and inhibit chondrocyte ferroptosis and cartilage matrix degradation by regulating P53, SLC7A11, and GPX4.
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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.