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REVIEW article

Front. Cell Dev. Biol.
Sec. Cell Death and Survival
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1510390
This article is part of the Research Topic Ferroptosis: Intersections, Implications, and Innovations in Programmed Cell Death View all 8 articles

Ferroptosis and Its Role in Osteoarthritis: Mechanisms, Biomarkers, and Therapeutic Perspectives

Provisionally accepted
Shanyu Lu Shanyu Lu 1Zhenyu Liu Zhenyu Liu 1Meiling Qi Meiling Qi 1Yingchao Wang Yingchao Wang 1Le Chang Le Chang 1Xiaolong Bai Xiaolong Bai 1Yingguang Jiao Yingguang Jiao 1Xinyao Chen Xinyao Chen 1Junping Zhen Junping Zhen 2*
  • 1 Second Hospital of Shanxi Medical University, Taiyuan, China
  • 2 Molecular imaging laboratory, Second Hospital of Shanxi Medical University, Taiyuan, China

The final, formatted version of the article will be published soon.

    Osteoarthritis (OA) is one of the leading causes of disability worldwide, characterized by a complex pathological process involving cartilage degradation, synovial inflammation, and subchondral bone remodeling. In recent years, ferroptosis, a form of programmed cell death driven by iron-dependent lipid peroxidation, has been recognized as playing a critical role in the onset and progression of OA. Investigating the molecular mechanisms of ferroptosis and its involvement in OA may offer novel strategies for diagnosing and treating this disease. This review first outlines the core mechanisms of ferroptosis, with a particular focus on the roles of critical molecules such as Glutathione Peroxidase 4 (GPX4), Transferrin Receptor 1 (TfR1), and Nuclear Receptor Coactivator 4 (NCOA4). Subsequently, this study examines the specific impacts of ferroptosis on the pathophysiology of OA. Building on this, the potential of ferroptosis-related biomarkers for OA diagnosis and treatment is highlighted, along with proposed therapeutic strategies targeting ferroptosis regulation. This review aims to deepen the understanding of ferroptosis mechanisms and advance the clinical application of regulatory therapies for OA.

    Keywords: Osteoarthritis, ferroptosis, Molecular mechanisms, biomarkers, therapeutic strategies

    Received: 12 Oct 2024; Accepted: 04 Dec 2024.

    Copyright: © 2024 Lu, Liu, Qi, Wang, Chang, Bai, Jiao, Chen and Zhen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Junping Zhen, Molecular imaging laboratory, Second Hospital of Shanxi Medical University, Taiyuan, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.