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The role of small leucine-rich proteoglycans in osteoarthritis pathogenesis

机译:小亮氨酸富含蛋白多糖在骨关节炎发病机制中的作用

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摘要

Objective: To give an overview of the literature on the role of small leucine-rich proteoglycans (SLRPs) in osteoarthritis (OA) pathogenesis. Method: A literature search was performed and reviewed using the narrative approach. Results: (1) OA is an organ disease with many tissue types and specific roles for each in the pathogenic process. (2) Key biological functions of SLRPs include interacting with collagens to modulate fibril formation, and binding various cell surface receptors and growth factors to influence cellular functions; (3) Accumulating evidence has demonstrated the involvement of SLRPs in OA pathogenesis, most of which came from SLRP-deficient mice models; (4) Possible mechanisms for SLRPs being involved in OA pathogenic process include their roles in the extracellular collagen network, TGF-β signaling pathways, subchondral bone, muscle weakness, and the innate immune inflammation; (5) SLRP-deficient mice offer a potential to understand the molecular mechanisms of OA initiation and progression. (6) Targeting SLRPs may offer a new therapeutic modality for OA through controlling and modifying the TGF-β-ECM system. (7) Monitoring SLRP fragmentation may be a promising biomarker strategy to evaluate OA status. Conclusions: Recent literature has shown that SLRPs may play an important role in OA pathogenesis. Possible mechanisms by which SLRPs are involved in this process have also been proposed. However, further investigations are needed in this field to better understand its mechanisms, develop treatments to slow down the degenerative process, and explore new approaches for effective and timely diagnosis of OA.
机译:目的:举行关于小亮氨酸富含蛋白多糖(SLRPS)在骨关节炎(OA)发病机制中的作用的文献概述。方法:使用叙述方法进行文献搜索并审查。结果:(1)OA是一种器官疾病,具有许多组织类型和各种组织类型的致病方法。 (2)SLRP的关键生物功能包括与胶原蛋白相互作用以调节原纤维形成,并结合各种细胞表面受体和生长因子以影响细胞功能; (3)积累证据表明,SLRP参与OA发病机制,其中大部分来自SLRP缺陷的小鼠模型; (4)涉及OA致病方法的SLRP的可能机制包括它们在细胞外胶原蛋白网络中的作用,TGF-β信号通路,骨髓内骨,肌肉弱点和先天免疫炎症; (5)SLRP缺陷小鼠提供了理解OA启动和进展的分子机制的可能性。 (6)靶向SLRP可以通过控制和修改TGF-β-ECM系统来提供OA的新治疗方式。 (7)监测SLRP碎片可能是评估OA状态的有前途的生物标志物策略。结论:最近的文献表明,SLRPS可能在OA发病机制中发挥重要作用。还提出了SLRPS参与该过程的可能机制。然而,在该领域需要进一步调查以更好地了解其机制,发展治疗,减缓退行性过程,并探索有效和及时诊断OA的新方法。

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