ArticleImmunity, inflammation and disease2023
High-fat diet aggravates the severity of the in vitro posttraumatic osteoarthritis model through macrophagic FBW7.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- RETRACTION: Downregulation of the Proton-Activated Cl- Channel TMEM206 Inhibits Malignant Properties of Human Osteosarcoma Cells.Oxidative medicine and cellular longevity · 2025Article
- Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024Review
- High-fat diet aggravates the severity of the in vitro posttraumatic osteoarthritis model through macrophagic FBW7.Immunity, inflammation and disease · 2023Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a prevalent and distressing chronic degenerative joint disorder characterized by damaged articular cartilage and inflamed joints. Among risk factors, obesity has emerged as the second-leading contributor to OA after age. Obesity is believed to play a key role in the development and progression of OA. This study aimed to investigate the role and underlying mechanisms of high-fat diet (HFD)-induced obesity in the development of OA. Our findings revealed that HFD could aggravate the destabilization of the medial meniscus (DMM)-induced damage in the mouse model of obesity. Similar results were observed when macrophages obtained from HFD-fed mice were cocultured with cartilage and subsequently stimulated with interleukin-1β (IL-1β). Mechanistically, we observed a decrease in the expression of intraarticular macrophagic FBW7, which was implicated in the aggravation of OA in the HFD-fed animal. Furthermore, by modulating the immune status of macrophages, we found that reversing the macrophagic expression of FBW7 in these cells can alleviate the chondrocyte damage. In conclusion, this study provides novel insights into the pathological mechanisms underlying HFD-related OA development by identifying the role of FBW7 in synovial macrophages. These findings open up new avenues for research and therapeutic interventions targeting HFD-related OA.
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