ArticleBone & joint research2019
Activation of the leptin pathway by high expression of the long form of the leptin receptor (Ob-Rb) accelerates chondrocyte senescence in osteoarthritis.
Article in Bone & joint research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed.
- Impact of a durable left ventricular assist device on inflammation and cardiac remodelling in subjects with advanced heart failure.Open heart · 2026Observational
- The perineurium integrates leptin with its sympathetic outflow to protect against obesity.Nature metabolism · 2026Article
- Sympathetic regulation of bone homeostasis and remodeling: molecular mechanisms, pathophysiological roles, and therapeutic implications.Frontiers in immunology · 2026Review
- Molecular mechanisms and therapeutic implications of the sympathetic nervous system in bone-related disorders: a brain-bone axis perspective.Bone research · 2025Review
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- Modulation of senescent LeprStem cell research & therapy · 2025Article
- Identification and analysis of immune aging related biomarkers in cartilage and meniscus tissues of osteoarthritis.American journal of clinical and experimental immunology · 2025Article
- Metabolism-Related Adipokines and Metabolic Diseases: Their Role in Osteoarthritis.Journal of inflammation research · 2025Review
- Regulating lipid metabolism in osteoarthritis: a complex area with important future therapeutic potential.Annals of medicine · 2024Review
- Ubiquitination and deubiquitination: Implications for the pathogenesis and treatment of osteoarthritis.Journal of orthopaedic translation · 2024Review
- Novel perspectives on leptin in osteoarthritis: Focus on aging.Genes & diseases · 2024Review
- Review
- Beyond mechanical loading: The metabolic contribution of obesity in osteoarthritis unveils novel therapeutic targets.Heliyon · 2023Review
- Leptin in Osteoarthritis and Rheumatoid Arthritis: Player or Bystander?International journal of molecular sciences · 2022Review
- Oral administration of live combinedFrontiers in microbiology · 2022Article
- Senomorphic agent pterostilbene ameliorates osteoarthritis through the PI3K/AKT/NF-κB axis: an in vitro and in vivo study.American journal of translational research · 2022Article
- Intra-articular low-dose parathyroid hormone (1-34) improves mobility and articular cartilage quality in a preclinical age-related knee osteoarthritis model.Bone & joint research · 2021Article
- Clinical evaluation after matrix-associated autologous chondrocyte transplantation : a comparison of four different graft types.Bone & joint research · 2021Article
- PARP-1 inhibition attenuates the inflammatory response in the cartilage of a rat model of osteoarthritis.Bone & joint research · 2021Article
- An Update on the Role of Leptin in the Immuno-Metabolism of Cartilage.International journal of molecular sciences · 2021Review
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6 authors.
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Abstract
objectivesActivation of the leptin pathway is closely correlated with human knee cartilage degeneration. However, the role of the long form of the leptin receptor (Ob-Rb) in cartilage degeneration needs further study. The aim of this study was to determine the effect of increasing the expression of Ob-Rb on chondrocytes using a lentiviral vector containing Ob-Rb.
methodsThe medial and lateral cartilage samples of the tibial plateau from 12 osteoarthritis (OA) patients were collected. Ob-Rb messenger RNA (mRNA) was detected in these samples. The Ob-Rb-overexpressing chondrocytes and controls were treated with different doses of leptin for two days. The activation of the p53/p21 pathway and the number of senescence-associated β-galactosidase (SA-β-gal)-positive cells were evaluated. The mammalian target of rapamycin (mTOR) signalling pathway and autophagy were detected after the chondrocytes were treated with a high dose of leptin.
resultsIn total, 12 cases were found to have severe medial cartilage wear compared with the lateral cartilage. Immunofluorescence showed that the expression of Ob-Rb in the medial cartilage of the tibial plateau was high. High levels of leptin led to cell cycle arrest and inhibited autophagy. After overexpression of Ob-Rb, the physiological dose of leptin induced cell senescence in the chondrocytes. High doses of leptin inhibited autophagy by activating the mTOR signalling pathway. Blockade of the mTOR signalling pathway could restore autophagy and partially reverse senescence induced by leptin in chondrocytes.
conclusionIn summary, the present study demonstrated that high doses of leptin induce cell senescence by activating the mTOR pathway in chondrocytes from OA cartilage. Highly expressed Ob-Rb accelerates chondrocyte senescence by activating the leptin pathway in OA.
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