ArticleJournal of orthopaedic surgery and research2023
PPARγ activation suppresses chondrocyte ferroptosis through mitophagy in osteoarthritis.
Article in Journal of orthopaedic surgery and research, 2023. 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, 35 citations in OpenAlex.
- PLA2G2F suppresses ferroptosis through phospholipid remodeling.Nature structural & molecular biology · 2026Article
- Mechanistic Links Underlying the Comorbidity of Osteoporosis and Osteoarthritis: Cell Fate Plasticity Driven by the Subchondral Bone Microenvironment.International journal of molecular sciences · 2026Review
- Bacteroides-derived endocannabinoid-like commendamide attenuates skeletal muscle ferroptosis in vitro: implications for Duchenne muscular dystrophy.Journal of translational medicine · 2026Article
- NSDHL as a regulator of lipid peroxidation and ER stress-mediated apoptosis in ovarian cancer.Biology direct · 2026Article
- Aging at the Crossroads of Cuproptosis and Ferroptosis: From Molecular Pathways to Age-Related Pathologies and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Mitochondrial quality control modulating chondrocyte behavior and fate in knee osteoarthritis: mechanistic insights and therapeutic prospects.Frontiers in immunology · 2026Review
- The dual role of autophagy in cartilage degradation: from mechanisms to targeted therapeutics.Frontiers in cell and developmental biology · 2026Review
- Lipid-Driven Immunometabolism in Mesenchymal Stromal Cells: A New Axis for Musculoskeletal Regeneration.International journal of molecular sciences · 2025Review
- Dehydrotanshinone II A alleviates osteoarthritis via activating PPARγ to inhibit ferroptosis in chondrocytes.Scientific reports · 2025Article
- An emerging role of mitochondrial quality control in bone metabolism: from molecular mechanisms to targeted therapeutic interventions.Cellular and molecular life sciences : CMLS · 2025Review
- VMP1 attenuates ferroptosis and mitochondrial dysfunction in nucleus pulposus cells through the PINK1/Parkin-mediated mitophagy pathway.Journal of orthopaedic surgery and research · 2025Article
- Epigenetic mechanisms of Nsd1-mediated histone methylation modifications in chondrocyte ferroptosis in knee osteoarthritis.Biomolecules & biomedicine · 2025Article
- Ferroptosis contributes to immunosuppression.Frontiers of medicine · 2025Review
- Integrated Bioinformatics and Experimental Validation Reveal Macrophage Polarization-Related Biomarkers for Osteoarthritis Diagnosis.Journal of multidisciplinary healthcare · 2025Article
- RETRACTED: PTEN Deficiency Induced by Extracellular Vesicle miRNAs fromInternational journal of molecular sciences · 2024Article
- Ferroptosis in Arthritis: Driver of the Disease or Therapeutic Option?International journal of molecular sciences · 2024Review
- Function and Mechanism of Abscisic Acid on Microglia-Induced Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2024Review
- PDK4 inhibits osteoarthritis progression by activating the PPAR pathway.Journal of orthopaedic surgery and research · 2024Article
- Potential therapies for HCC involving targeting the ferroptosis pathway.American journal of cancer research · 2024Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundOsteoarthritis (OA) is a prevalent disease plaguing the elderly. Recently, chondrocyte ferroptosis has been demonstrated to promote the progression of OA. Peroxisome proliferator-activated receptor-γ (PPARγ) is an important factor in maintaining cartilage health. However, the relationship between PPARγ and chondrocyte ferroptosis in OA and its mechanism is completely unclear.
methodsWe established a surgically induced knee OA rat model to investigate PPARγ and chondrocyte ferroptosis in OA. Rat knee specimens were collected for Safranin O/Fast Green staining and immunohistochemical staining after administered orally placebo or pioglitazone (PPARγ agonist) for 4 weeks. We used RSL3 to establish a chondrocyte ferroptosis model cultured in vitro to study the role of PPARγ activation toward ferroptosis, mitochondrial function, and PTEN-induced putative kinase 1 (Pink1)/Parkin-dependent mitophagy. GW9662 (PPARγ antagonist), Mdivi-1 (mitophagy inhibitor), and chloroquine (mitophagy inhibitor) were employed to investigate the mechanism of PPARγ-Pink1/Parkin-dependent mitophagy in the inhibition of ferroptosis.
resultsWe found that PPARγ activation by pioglitazone attenuated not only OA but also inhibited the expression of the ferroptosis marker acyl-CoA synthetase long-chain family member 4 (ACSL4) at the same time in rats. Furthermore, in vivo and in vitro data indicated that PPARγ activation restored Pink1/Parkin-dependent mitophagy, improved mitochondrial function, inhibited chondrocyte ferroptosis, and delayed the progression of OA.
conclusionsThe present study demonstrated that PPARγ activation attenuates OA by inhibiting chondrocyte ferroptosis, and this chondroprotective effect was achieved by promoting the Pink1/Parkin-dependent mitophagy pathway.
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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 Socratic graph.