AUTHOR=Cao Siyang , Wei Yihao , Xu Huihui , Weng Jian , Qi Tiantian , Yu Fei , Liu Su , Xiong Ao , Liu Peng , Zeng Hui 
  
TITLE=Crosstalk between ferroptosis and chondrocytes in osteoarthritis: a systematic review of in vivo and in vitro studies
  
JOURNAL=Frontiers in Immunology
  
VOLUME=Volume 14 - 2023
  
YEAR=2023
  
URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2023.1202436
  
DOI=10.3389/fimmu.2023.1202436
  
ISSN=1664-3224
  
ABSTRACT=Ferroptosis is a novel form of programmed cell death described as the iron-dependent accumulation of lipid hydroperoxides. Since its initial description in 2012, there has been mounting interest in the function and regulation of ferroptosis. Recent scientific reports have revealed that ferroptosis is closely associated with 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. A rigorous systematic review (SR) following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines was performed to find the interplay between ferroptosis and chondrocytes in OA. The systematic search was computed employing Embase, Ovid, ProQuest, PubMed, Scopus, the Cochrane Library and Web of Science to identify studies conducted from the inception of the respective databases up to January 31st, 2023. Based upon the results of the literature search, 21 studies that met the relevant criteria were deemed eligible and incorporated into the present up-to-date SR. Multiple biological phenomena, including mitochondrial dysfunction, dysregulated iron metabolism, oxidative stress and key signalling pathways, are involved in the processes associated with chondrocyte ferroptosis entailing OA development. 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.