PDF(Pubmed)
Abstract：
Recent scientific reports have revealed a close association between ferroptosis and the occurrence and development of osteoarthritis (OA). Nevertheless, the precise mechanisms by which ferroptosis influences OA and how to hobble OA progression by inhibiting chondrocyte ferroptosis have not yet been fully elucidated. This study aims to conduct a comprehensive systematic review (SR) to address these gaps.
Following the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020, we conducted a comprehensive search of the Embase, Ovid, ProQuest, PubMed, Scopus, the Cochrane Library, and Web of Science databases to identify relevant studies that investigate the association between ferroptosis and chondrocytes in OA. Our search included studies published from the inception of these databases until January 31st, 2023. Only studies that met the predetermined quality criteria were included in this SR.
In this comprehensive SR, a total of 21 studies that met the specified criteria were considered suitable and included in the current updated synthesis. The mechanisms underlying chondrocyte ferroptosis and its association with OA progression involve various biological phenomena, including mitochondrial dysfunction, dysregulated iron metabolism, oxidative stress, and crucial signaling pathways.
Ferroptosis in chondrocytes has opened an entirely new chapter for the investigation of OA, and targeted regulation of it is springing up as an attractive and promising therapeutic tactic for OA.
https://inplasy.com/inplasy-2023-3-0044/, identifier INPLASY202330044.
Following the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020, we conducted a comprehensive search of the Embase, Ovid, ProQuest, PubMed, Scopus, the Cochrane Library, and Web of Science databases to identify relevant studies that investigate the association between ferroptosis and chondrocytes in OA. Our search included studies published from the inception of these databases until January 31st, 2023. Only studies that met the predetermined quality criteria were included in this SR.
In this comprehensive SR, a total of 21 studies that met the specified criteria were considered suitable and included in the current updated synthesis. The mechanisms underlying chondrocyte ferroptosis and its association with OA progression involve various biological phenomena, including mitochondrial dysfunction, dysregulated iron metabolism, oxidative stress, and crucial signaling pathways.
Ferroptosis in chondrocytes has opened an entirely new chapter for the investigation of OA, and targeted regulation of it is springing up as an attractive and promising therapeutic tactic for OA.
https://inplasy.com/inplasy-2023-3-0044/, identifier INPLASY202330044.
摘要：
■最近的科学报告揭示了铁性凋亡与骨关节炎（OA）的发生和发展之间的密切关系。然而，铁性凋亡影响OA的确切机制以及如何通过抑制软骨细胞铁性凋亡阻碍OA的进展尚未完全阐明.本研究旨在进行全面的系统评价(SR)来解决这些差距。
■遵循2020年系统审查和荟萃分析（PRISMA）的首选报告项目指南，我们对Embase进行了全面搜索，奥维德,ProQuest,PubMed,Scopus,Cochrane图书馆,和WebofScience数据库来确定相关研究，以调查OA中铁细胞凋亡与软骨细胞之间的关系。我们的搜索包括从这些数据库开始到1月31日发表的研究，2023年。只有符合预定质量标准的研究才包括在此SR中。
■在这个全面的SR中，共有21项符合规定标准的研究被认为是合适的,并纳入了最新的综合报告.软骨细胞铁性凋亡及其与OA进展的关系的机制涉及各种生物学现象，包括线粒体功能障碍,铁代谢失调，氧化应激，和关键的信号通路。
■软骨细胞的铁凋亡为OA的研究开辟了一个全新的篇章，对其进行有针对性的调节正在兴起，成为一种有吸引力和有前途的OA治疗策略。
■https://inplasy.com/inplasy-2023-3-0044/,标识符INPLASY202330044。
■遵循2020年系统审查和荟萃分析（PRISMA）的首选报告项目指南，我们对Embase进行了全面搜索，奥维德,ProQuest,PubMed,Scopus,Cochrane图书馆,和WebofScience数据库来确定相关研究，以调查OA中铁细胞凋亡与软骨细胞之间的关系。我们的搜索包括从这些数据库开始到1月31日发表的研究，2023年。只有符合预定质量标准的研究才包括在此SR中。
■在这个全面的SR中，共有21项符合规定标准的研究被认为是合适的,并纳入了最新的综合报告.软骨细胞铁性凋亡及其与OA进展的关系的机制涉及各种生物学现象，包括线粒体功能障碍,铁代谢失调，氧化应激，和关键的信号通路。
■软骨细胞的铁凋亡为OA的研究开辟了一个全新的篇章，对其进行有针对性的调节正在兴起，成为一种有吸引力和有前途的OA治疗策略。
■https://inplasy.com/inplasy-2023-3-0044/,标识符INPLASY202330044。
