Department of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Front Endocrinol (Lausanne). 2024 May 24;15:1393550. doi: 10.3389/fendo.2024.1393550. eCollection 2024.
Osteoarthritis (OA) is an intricate pathological condition that primarily affects the entire synovial joint, especially the hip, hand, and knee joints. This results in inflammation in the synovium and osteochondral injuries, ultimately causing functional limitations and joint dysfunction. The key mechanism responsible for maintaining articular cartilage function is chondrocyte metabolism, which involves energy generation through glycolysis, oxidative phosphorylation, and other metabolic pathways. Some studies have shown that chondrocytes in OA exhibit increased glycolytic activity, leading to elevated lactate production and decreased cartilage matrix synthesis. In OA cartilage, chondrocytes display alterations in mitochondrial activity, such as decreased ATP generation and increased oxidative stress, which can contribute to cartilage deterioration. Chondrocyte metabolism also involves anabolic processes for extracellular matrix substrate production and energy generation. During OA, chondrocytes undergo considerable metabolic changes in different aspects, leading to articular cartilage homeostasis deterioration. Numerous studies have been carried out to provide tangible therapies for OA by using various models and targeting chondrocyte metabolism, although there are still certain limitations. With growing evidence indicating the essential role of chondrocyte metabolism in disease etiology, this literature review explores the metabolic characteristics and changes of chondrocytes in the presence of OA, both and . To provide insight into the complex metabolic reprogramming crucial in chondrocytes during OA progression, we investigate the dynamic interaction between metabolic pathways, such as glycolysis, lipid metabolism, and mitochondrial function. In addition, this review highlights prospective future research directions for novel approaches to diagnosis and treatment. Adopting a multifaceted strategy, our review aims to offer a comprehensive understanding of the metabolic intricacies within chondrocytes in OA, with the ultimate goal of identifying therapeutic targets capable of modulating chondrocyte metabolism for the treatment of OA.
骨关节炎(OA)是一种复杂的病理状况,主要影响整个滑膜关节,特别是髋关节、手和膝关节。这会导致滑膜炎症和骨软骨损伤,最终导致功能受限和关节功能障碍。维持关节软骨功能的关键机制是软骨细胞代谢,它涉及通过糖酵解、氧化磷酸化和其他代谢途径产生能量。一些研究表明,OA 中的软骨细胞表现出增加的糖酵解活性,导致乳酸产量增加和软骨基质合成减少。在 OA 软骨中,软骨细胞的线粒体活性发生改变,例如 ATP 生成减少和氧化应激增加,这可能导致软骨恶化。软骨细胞代谢还涉及细胞外基质底物产生和能量生成的合成代谢过程。在 OA 中,软骨细胞在不同方面经历相当大的代谢变化,导致关节软骨稳态恶化。已经进行了许多研究,通过使用各种模型和针对软骨细胞代谢,为 OA 提供切实可行的治疗方法,尽管仍然存在某些限制。越来越多的证据表明软骨细胞代谢在疾病发病机制中的重要作用,本文献综述探讨了 OA 存在时软骨细胞的代谢特征和变化。为了深入了解 OA 进展过程中软骨细胞中复杂的代谢重编程,我们研究了代谢途径之间的动态相互作用,如糖酵解、脂质代谢和线粒体功能。此外,本综述还强调了用于诊断和治疗的新型方法的未来研究方向。本综述采用多方面的策略,旨在全面了解 OA 中软骨细胞的代谢复杂性,最终确定能够调节软骨细胞代谢以治疗 OA 的治疗靶点。