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线粒体代谢在骨关节炎中的作用和干预。

The role and intervention of mitochondrial metabolism in osteoarthritis.

机构信息

Department of Orthopedics, The 960th hospital of the Joint Logistics Support Force of the People's Liberation Army, Jinan, Shandong, China.

Department of Orthopedics, Jinan City People's Hospital, Jinan, Shandong, China.

出版信息

Mol Cell Biochem. 2024 Jun;479(6):1513-1524. doi: 10.1007/s11010-023-04818-9. Epub 2023 Jul 24.

Abstract

Osteoarthritis (OA), a prevalent degenerative joint disease, affects a substantial global population. Despite the elusive etiology of OA, recent investigations have implicated mitochondrial dysfunction as a significant factor in disease pathogenesis. Mitochondria, pivotal cellular organelles accountable for energy production, exert essential roles in cellular metabolism. Hence, mitochondrial dysfunction can exert broad-ranging effects on various cellular processes implicated in OA development. This comprehensive review aims to provide an overview of the metabolic alterations occurring in OA and elucidate the diverse mechanisms through which mitochondrial dysfunction can contribute to OA pathogenesis. These mechanisms encompass heightened oxidative stress and inflammation, perturbed chondrocyte metabolism, and compromised autophagy. Furthermore, this review will explore potential interventions targeting mitochondrial metabolism as means to impede or decelerate the progression of OA. In summary, this review offers a comprehensive understanding of the involvement of mitochondrial metabolism in OA and underscores prospective intervention strategies.

摘要

骨关节炎(OA)是一种常见的退行性关节疾病,影响着全球相当大的一部分人群。尽管 OA 的病因难以捉摸,但最近的研究表明线粒体功能障碍是疾病发病机制中的一个重要因素。线粒体是负责能量生产的关键细胞细胞器,在细胞代谢中发挥着重要作用。因此,线粒体功能障碍会对 OA 发展中涉及的各种细胞过程产生广泛的影响。本综述旨在概述 OA 中发生的代谢变化,并阐明线粒体功能障碍如何通过多种机制导致 OA 发病机制。这些机制包括氧化应激和炎症增加、软骨细胞代谢紊乱以及自噬受损。此外,本综述还将探讨针对线粒体代谢的潜在干预措施,作为阻止或减缓 OA 进展的手段。总之,本综述提供了对线粒体代谢在 OA 中的作用的全面理解,并强调了有前景的干预策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87b5/11224101/7dc495b5a946/11010_2023_4818_Fig1_HTML.jpg

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