Cross-regulation of inflammation and metabolic mechanisms in osteoarthritis: recent advances bridging the gap to novel treatments

骨关节炎中炎症和代谢机制的交叉调控:最新进展为新型治疗铺平道路

阅读:1

Abstract

Osteoarthritis (OA) is a debilitating degenerative disease of the joints and one of the most prevalent joint disorders affecting millions of individuals worldwide. This disease is highlighted by significant morbidity owing to encumbering joint pain and functional impairment. OA ensues following disruption of normal homeostasis in the joint resulting from aging, metabolic changes, or as a consequence of joint injury (referred to as post-traumatic OA). These processes are largely driven by low-grade inflammation that gradually compromises the anabolic and protective activities of joint resident cells including chondrocytes, synovial fibroblasts (SFs) and immune cells. Ample research suggests that the process of cartilage deterioration is the endpoint of complex pathologic processes culminating with synovitis, subchondral bone sclerosis, osteophyte formation, aberrant remodeling, and ultimately articular cartilage degradation. There remains a great need for identifying early markers and a "window of opportunity" to enable timely interventions in OA. However, this effort is hampered by the complex nature of the disease and its comorbidities. Joint holistic approaches using recent unbiased multi-omic tools are currently at the forefront promising better understanding of OA development. Currently, there are no meaningful disease-modifying drugs to treat OA, with surgical procedures as the ultimate effective intervention for end stage OA patients. The disability, pain, and surgical costs associated with OA management position this disease among the costliest and onerous for our society. This mini review will highlight advances in the last two decades and major obstacles limiting progress in OA research with particular emphasis on metabolic and inflammatory comorbidities.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。