ROS-Dependent Lipid Peroxidation and Reliant Antioxidant Ferroptosis-Suppressor-Protein 1 in Rheumatoid Arthritis: a Cov
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REVIEW
ROS-Dependent Lipid Peroxidation and Reliant Antioxidant Ferroptosis-Suppressor-Protein 1 in Rheumatoid Arthritis: a Covert Clue for Potential Therapy Zhaoxiang Xie ,1,2 Haodong Hou,2 Dan Luo,3 Ran An,2 Yunpeng Zhao,1,4 and Cheng Qiu1,2,4
(Received May 18,2020; accepted Sember 2,2020)
Abstract— Rheumatoid arthritis (RA) is a common systemic autoimmune disease with
a prevalence of about 1% in which genetic and environmental risk factors both participate in performance of disease. Though several studies contributed in identifying its etiology and pathogenesis, the underlying mechanisms are still unknown. To date, so as palliative for RA, cure strategies are still popular. Hypoxia and oxidative stress are implicated to RA development and subsequent ROS-mediated cell death which is a critical feature for RA progression. As for cell death and lipid peroxidation, ferroptosis is a newly discovered, iron-dependent, and non-apoptotic cell death which draws various attention due to its potential strategies for cancer therapy. Meanwhile, ferroptosis-suppressor-protein 1 (FSP1) is recently identified as a seminal breakthrough owing to its property of versus ferroptosis. By virtue of the complicated research progress on FSP1 with ferroptosis, in this review, we summarize the whole region of relevance between ROS and RA. Taken together, we hypothesize that ROS accompanied with ferroptosis may function as a reciprocal with cell death that interplays with RA; besides, FSP1 might become a potential therapeutic target for RA because of its potential interaction with TNF-α/ROS1
Department of Orthopaedic Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, People’s Republic of China 2 Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, People’s Republic of China 3 College of Stomatology, Qingdao University, Qingdao, 266071, Shandong, People’s Republic of China 4 To whom correspondence should be addressed to Yunpeng Zhao at Department of Orthopaedic Surgery, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, 250012, Shandong, People’s Republic of China. E-mail: [email protected]; and ; [email protected]
0360-3997/20/0000-0001/0 # 2020 Springer Science+Business Media, LLC, part of Springer Nature
Xie, Hou, Luo, An, Zhao, and Qiu positive feedback loop. This review systematically concludes the previous understandings about identification of ROS and FSP1 and, in turn, aims to provide references for further achievements of them and hints on elucidation of its thorough underlying mechanisms. KEY WORDS: rheumatoid arthritis; ROS; cell death; ferroptosis; FSP1; TNF-α.
INTRODUCTION In recent years, rheumatoid arthritis (RA) vaults into one of the common diseases which afflict 0.5–1% of populations all over the world and bring economic burden for both individual and society [1]. However, current medical strategies only provide symptomatic relief but fail to cure it completely or halt this progression [2, 3]. RA is a complex systemic d
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