ArticleImmune network2024
Oxidized LDL Accelerates Cartilage Destruction and Inflammatory Chondrocyte Death in Osteoarthritis by Disrupting the TFEB-Regulated Autophagy-Lysosome Pathway.
Article in Immune network, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Endocrine‑metabolic imbalance drives osteoarthritis: From whole‑joint pathobiology to precision therapy (Review).International journal of molecular medicine · 2026Review
- Association of serum Wnt1-inducible signaling pathway protein 1 (WISP1) levels with osteoarthritis and obesity-related inflammation in obese adults.Scientific reports · 2026Article
- Metabolic dysfunction-associated fatty liver disease and risk of knee osteoarthritis: A prospective cohort study.Clinical and experimental medicine · 2026Article
- Regulated Cell Death Pathways in Chondrocytes During Septic Arthritis: Current Evidence and Future Perspectives.Journal of inflammation research · 2026Review
- Focus on necroptosis: its role in the pathogenesis and therapeutic potential of osteoarthritis.Frontiers in immunology · 2026Review
- Phosphatidylethanolamine Alleviates Osteoarthritis Progression by Inhibiting Oxidative Stress-Induced Chondrocyte Ferroptosis in a Lysosomal-Dependent Manner.International journal of general medicine · 2026Article
- Lipid metabolic reprogramming in osteoarthritis: cartilage-centered mechanisms, whole-joint interactions, and therapeutic challenges.Frontiers in endocrinology · 2026Review
- Chinese Massage (Tuina) Attenuates Knee Osteoarthritis by Modulating Autophagy-Related Cytokines: A Multidisciplinary Methodological Investigation.Journal of inflammation research · 2025Article
- Association of organs-crosstalk with the pathogenesis of osteoarthritis: cartilage as a key player.Frontiers in endocrinology · 2025Review
- Beyond cardiovascular disease: remnant cholesterol as a novel risk factor for osteoarthritis.Frontiers in nutrition · 2025Article
- Exploring the Interconnection between Metabolic Dysfunction and Gut Microbiome Dysbiosis in Osteoarthritis: A Narrative Review.Biomedicines · 2024Review
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
Osteoarthritis (OA) involves cartilage degeneration, thereby causing inflammation and pain. Cardiovascular diseases, such as dyslipidemia, are risk factors for OA; however, the mechanism is unclear. We investigated the effect of dyslipidemia on the development of OA. Treatment of cartilage cells with low-density lipoprotein (LDL) enhanced abnormal autophagy but suppressed normal autophagy and reduced the activity of transcription factor EB (TFEB), which is important for the function of lysosomes. Treatment of LDL-exposed chondrocytes with rapamycin, which activates TFEB, restored normal autophagy. Also, LDL enhanced the inflammatory death of chondrocytes, an effect reversed by rapamycin. In an animal model of hyperlipidemia-associated OA, dyslipidemia accelerated the development of OA, an effect reversed by treatment with a statin, an anti-dyslipidemia drug, or rapamycin, which activates TFEB. Dyslipidemia reduced the autophagic flux and induced necroptosis in the cartilage tissue of patients with OA. The levels of triglycerides, LDL, and total cholesterol were increased in patients with OA compared to those without OA. The C-reactive protein level of patients with dyslipidemia was higher than that of those without dyslipidemia after total knee replacement arthroplasty. In conclusion, oxidized LDL, an important risk factor of dyslipidemia, inhibited the activity of TFEB and reduced the autophagic flux, thereby inducing necroptosis in chondrocytes.
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