Crosstalk between ferroptosis and chondrocytes in osteoarthritis: a systematic review of in vivo and in vitro studies

Front Immunol. 2023 Jul 14:14:1202436. doi: 10.3389/fimmu.2023.1202436. eCollection 2023.

Abstract

Purpose: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

Systematic review registration: https://inplasy.com/inplasy-2023-3-0044/, identifier INPLASY202330044.

Keywords: chondrocytes; crosstalk; ferroptosis; osteoarthritis; systematic review.

Publication types

  • Systematic Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Chondrocytes / metabolism
  • Ferroptosis*
  • Humans
  • Osteoarthritis* / metabolism
  • Oxidative Stress
  • Signal Transduction

Grants and funding

Grants for this study were provided by the National Natural Science Foundation of China (No. 82172432; No. 82102568 and No. 82001319); the National & Local Joint Engineering Research Centre of Orthopaedic Biomaterials (No. XMHT20190204007); the Guangdong Basic and Applied Basic Research Foundation (No. 2021A1515012586; No. 2021A1515220054; No. 2022B1515120046; No. 2022A1515220038; No. 2022A1515220111; No. 2021A1515220037; No. 2022A1515220165); the Shenzhen High-Level Hospital Construction Fund, the Shenzhen Key Medical Discipline Construction Fund (No. SZXK023); the Shenzhen ‘San-Ming’ Project of Medicine (No. SZSM201612092); the Research and Development Projects of Shenzhen (No. KCXFZ20201221173411031; No. JCYJ20210324110214040; No. JCYJ20220531094214032; No. JCYJ20190809152409606; No. JCYJ20210324105806016); and the Scientific Research Foundation of Peking University Shenzhen Hospital (No. KYQD2021099).