ArticleBone research2018
Dietary fat-associated osteoarthritic chondrocytes gain resistance to lipotoxicity through PKCK2/STAMP2/FSP27.
Article in Bone research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Lipid metabolic reprogramming in osteoarthritis: cartilage-centered mechanisms, whole-joint interactions, and therapeutic challenges.Frontiers in endocrinology · 2026Review
- Novel near-infrared probe for monitoring lipid peroxidation-mediated viscosity change in ferroptotic hepatocytes.Clinical and molecular hepatology · 2026Article
- Dysfunctional autophagy triggers STING1 activation to exacerbate cartilage degeneration in obesity-associated osteoarthritis.Autophagy · 2025Article
- SESN2 maintains cartilage homeostasis by SREBP1-mediated lipid metabolism during osteoarthritis progression.iScience · 2025Article
- Regulating obesity-induced osteoarthritis by targeting p53-FOXO3, osteoclast ferroptosis, and mesenchymal stem cell adipogenesis.Nature communications · 2025Article
- Red blood cell exposure increases chondrocyte susceptibility to oxidative stress following hemarthrosis.Osteoarthritis and cartilage · 2023Article
- CircRREB1 mediates lipid metabolism related senescent phenotypes in chondrocytes through FASN post-translational modifications.Nature communications · 2023Article
- The Janus-Faced Role of Lipid Droplets in Aging: Insights from the Cellular Perspective.Biomolecules · 2023Review
- L-carnitine alleviates synovitis in knee osteoarthritis by regulating lipid accumulation and mitochondrial function through the AMPK-ACC-CPT1 signaling pathway.Journal of orthopaedic surgery and research · 2023Article
- An Integrated View of Stressors as Causative Agents in OA Pathogenesis.Biomolecules · 2023Review
- Equine osteoarthritis modifies fatty acid signatures in synovial fluid and its extracellular vesicles.Arthritis research & therapy · 2023Article
- Upregulated FOXM1 stimulates chondrocyte senescence in Acot12Theranostics · 2023Article
- Association Between Gut Microbiota and Osteoarthritis: A Review of Evidence for Potential Mechanisms and Therapeutics.Frontiers in cellular and infection microbiology · 2022Review
- Adiponectin, May Be a Potential Protective Factor for Obesity-Related Osteoarthritis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Review
- Article
- Synovial Fluid Fatty Acid Profiles Are Differently Altered by Inflammatory Joint Pathologies in the Shoulder and Knee Joints.Biology · 2021Article
- Fatty Acids and Oxylipins in Osteoarthritis and Rheumatoid Arthritis-a Complex Field with Significant Potential for Future Treatments.Current rheumatology reports · 2021Review
- CIDE Proteins in Human Health and Disease.Cells · 2019Review
- Mitophagy in Hepatic Insulin Resistance: Therapeutic Potential and Concerns.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Free fatty acids (FFAs), which are elevated with metabolic syndrome, are considered the principal offender exerting lipotoxicity. Few previous studies have reported a causal relationship between FFAs and osteoarthritis pathogenesis. However, the molecular mechanism by which FFAs exert lipotoxicity and induce osteoarthritis remains largely unknown. We here observed that oleate at the usual clinical range does not exert lipotoxicity while oleate at high pathological ranges exerted lipotoxicity through apoptosis in articular chondrocytes. By investigating the differential effect of oleate at toxic and nontoxic concentrations, we revealed that lipid droplet (LD) accumulation confers articular chondrocytes, the resistance to lipotoxicity. Using high fat diet-induced osteoarthritis models and articular chondrocytes treated with oleate alone or oleate plus palmitate, we demonstrated that articular chondrocytes gain resistance to lipotoxicity through protein kinase casein kinase 2 (PKCK2)-six-transmembrane protein of prostate 2 (STAMP2)-and fat-specific protein 27 (FSP27)-mediated LD accumulation. We further observed that the exertion of FFAs-induced lipotoxicity was correlated with the increased concentration of cellular FFAs freed from LDs, whether FFAs are saturated or not. In conclusion, PKCK2/STAMP2/FSP27-mediated sequestration of FFAs in LD rescues osteoarthritic chondrocytes. PKCK2/STAMP2/FSP27 should be considered for interventions against metabolic OA.
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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.