ROS-Dependent Lipid Peroxidation and Reliant Antioxidant Ferroptosis-Suppressor-Protein 1 in Rheumatoid Arthritis: a Covert Clue for Potential Therapy

Xie, Zhiang; Hou, Haodong; Luo, Dan; An, Ran; Zhao, Yunpeng; Qiu, Cheng

doi:10.1007/s10753-020-01338-2

Cited by 60 publications

(48 citation statements)

References 71 publications

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“…Iron is found in the synovial membrane of lesions and is known to be a catalyst for H 2 O 2 production of • OH via the Fenton reaction [ 38 ]. The degenerative process of RA development may be aided by lipid peroxidation-related ferroptosis [ 39 , 40 ]. Notably, sulfasalazine indirectly increases ferric iron levels, triggering the Fenton reaction, which produces excess lipid ROS and causes ferroptosis [ 41 ].…”

Section: The Production Of Ros In Synovitismentioning

confidence: 99%

The Role of Reactive Oxygen Species in the Rheumatoid Arthritis-Associated Synovial Microenvironment

et al. 2022

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Rheumatoid arthritis (RA) is an inflammatory disease that begins with a loss of tolerance to modified self-antigens and immune system abnormalities, eventually leading to synovitis and bone and cartilage degradation. Reactive oxygen species (ROS) are commonly used as destructive or modifying agents of cellular components or they act as signaling molecules in the immune system. During the development of RA, a hypoxic and inflammatory situation in the synovium maintains ROS generation, which can be sustained by increased DNA damage and malfunctioning mitochondria in a feedback loop. Oxidative stress caused by abundant ROS production has also been shown to be associated with synovitis in RA. The goal of this review is to examine the functions of ROS and related molecular mechanisms in diverse cells in the synovial microenvironment of RA. The strategies relying on regulating ROS to treat RA are also reviewed.

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Section: The Production Of Ros In Synovitismentioning

confidence: 99%

The Role of Reactive Oxygen Species in the Rheumatoid Arthritis-Associated Synovial Microenvironment

et al. 2022

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“…FSP1-mediated ferroptosis is also involved in inflammatory processes, hinting that ferroptosis is capable of recruiting immune cells in the tumor microenvironment ( 22 , 63 ). The interaction between osteosarcoma cells and antitumor drugs is complicated.…”

Section: Discussionmentioning

confidence: 99%

Novel Therapeutic Savior for Osteosarcoma: The Endorsement of Ferroptosis

et al. 2022

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Ferroptosis has recently been discovered as an iron-dependent and non-apoptotic regulated mechanism of cell death. The induction of ferroptosis in tumor cells improves tumor treatment, making it a current research hotspot. Mechanistically, it starts by lipid peroxidation, iron accumulation, reactive oxygen species (ROS) production, and glutathione deprivation, highlighting novel treatment opportunities for many tumors and neurodegenerative disorders. Several tumor cell lines are resistant to ferroptosis inducers, even when the ferroptosis key enzyme glutathione peroxidase 4 (GPX4) is blocked, indicating that other important elements are also involved in this process. Ferroptosis-suppressor-protein 1 (FSP1) was discovered to be one of these elements in addition to a few others such as ferroptotic gatekeepers like GTP cyclohydrolase 1 (GCH1) and dihydroorotate dehydrogenase (DHODH). Osteosarcoma is the most common primary malignant bone tumor observed most frequently in children and adolescents. Several studies demonstrated that ferroptosis plays a critical role in the treatment of osteosarcoma, in particular drug-resistant osteosarcoma cells. We outlined four primary regulators involved in ferroptosis in this article, reviewed previously published studies of ferroptosis in osteosarcoma to provide covert insights about osteosarcoma treatment, and highlighted several critical issues to point out future research possibilities.

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“…The FSP1-CoQ10 pathway can improve lipid peroxidation through free radical capture, and the process of ferroptosis is also blocked. Some studies speculate that FSP1 may improve RA through the TNF-a/ROS positive feedback loop (41,42). However, the specific contribution of ferroptosis as a mode of cell death was not addressed in these studies.…”

Section: Membrane Lipid Antioxidant Systemmentioning

confidence: 97%

Ferroptosis in Rheumatoid Arthritis: A Potential Therapeutic Strategy

Zhao

Yang

et al. 2022

Front. Immunol.

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Ferroptosis is one of the newly discovered forms of cell-regulated death characterized by iron-dependent lipid peroxidation. Extensive research has focused on the roles of ferroptosis in tumors, blood diseases, and neurological diseases. Some recent findings have indicated that ferroptosis may also be related to the occurrence and development of inflammatory arthritis. Ferroptosis may be a potential therapeutic target, and few studies in vitro and animal models have shown implications in the pathogenesis of inflammatory arthritis. This mini review discussed the common features between ferroptosis and the pathogenesis of rheumatoid arthritis (RA), and evaluated therapeutic applications of ferroptosis regulators in preclinical and clinical research. Some critical issues worth paying attention to were also raised to guide future research efforts.

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ROS-Dependent Lipid Peroxidation and Reliant Antioxidant Ferroptosis-Suppressor-Protein 1 in Rheumatoid Arthritis: a Covert Clue for Potential Therapy

Cited by 60 publications

References 71 publications

The Role of Reactive Oxygen Species in the Rheumatoid Arthritis-Associated Synovial Microenvironment

The Role of Reactive Oxygen Species in the Rheumatoid Arthritis-Associated Synovial Microenvironment

Novel Therapeutic Savior for Osteosarcoma: The Endorsement of Ferroptosis

Ferroptosis in Rheumatoid Arthritis: A Potential Therapeutic Strategy

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