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Pathobiology of obesity and osteoarthritis: integrating biomechanics and inflammation

机译:肥胖和骨关节炎的病理生物学:整合生物力学和炎症

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Obesity is a significant risk factor for developing osteoarthritis in weight-bearing and non-weight-bearing joints. Although the pathogenesis of obesity-associated osteoarthritis is not completely understood, recent studies indicate that pro-inflammatory metabolic factors contribute to an increase in osteoarthritis risk. Adipose tissue, and in particular infrapatellar fat, is a local source of pro-inflammatory mediators that are increased with obesity and have been shown to increase cartilage degradation in cell and tissue culture models. One adipokine in particular, leptin, may be a critical mediator of obesity-associated osteoarthritis via synergistic actions with other inflammatory cytokines. Biomechanical factors may also increase the risk of osteoarthritis by activating cellular inflammation and promoting oxidative stress. However, some types of biomechanical stimulation, such as physiologic cyclic loading, inhibit inflammation and protect against cartilage degradation. A high percentage of obese ind...
机译:肥胖是负重关节和非负重关节发展为骨关节炎的重要危险因素。尽管肥胖相关的骨关节炎的发病机理尚未完全明了,但最近的研究表明促炎性代谢因子导致骨关节炎的风险增加。脂肪组织,特别是pat下脂肪是促炎性介质的局部来源,其随着肥胖而增加,并且在细胞和组织培养模型中已显示出软骨降解的增加。一种肥胖因子,特别是瘦素,可能通过与其他炎性细胞因子的协同作用而成为肥胖相关骨关节炎的关键介质。生物力学因素还可能通过激活细胞炎症并促进氧化应激而增加骨关节炎的风险。但是,某些类型的生物力学刺激(例如生理循环负荷)会抑制炎症并保护软骨免于降解。肥胖的人比例很高

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