Ferroptosis in Arthritis: Driver of the Disease or Therapeutic Option?

被引:0
|
作者
Bieri, Shania [1 ]
Moller, Burkhard [2 ]
Amsler, Jennifer [2 ,3 ]
机构
[1] Univ Bern, Fac Med, CH-3012 Bern, Switzerland
[2] Univ Bern, Bern Univ Hosp, Dept Rheumatol & Immunol, CH-3010 Bern, Switzerland
[3] Univ Bern, Dept Biomed Res DBMR, CH-3008 Bern, Switzerland
关键词
ferroptosis; ROS; lipid peroxidation; iron; rheumatoid arthritis; osteoarthritis; RA-FLS; chondrocytes; RHEUMATOID-ARTHRITIS; CHONDROCYTE FERROPTOSIS; SYNOVIAL FIBROBLASTS; CELL-DEATH; SPONDYLOARTHRITIS; OSTEOARTHRITIS; MECHANISMS; CYTOKINES; CARTILAGE; STRESS;
D O I
10.3390/ijms25158212
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ferroptosis is a form of iron-dependent regulated cell death caused by the accumulation of lipid peroxides. In this review, we summarize research on the impact of ferroptosis on disease models and isolated cells in various types of arthritis. While most studies have focused on rheumatoid arthritis (RA) and osteoarthritis (OA), there is limited research on spondylarthritis and crystal arthropathies. The effects of inducing or inhibiting ferroptosis on the disease strongly depend on the studied cell type. In the search for new therapeutic targets, inhibiting ferroptosis in chondrocytes might have promising effects for any type of arthritis. On the other hand, ferroptosis induction may also lead to a desired decrease of synovial fibroblasts in RA. Thus, ferroptosis research must consider the cell-type-specific effects on arthritis. Further investigation is needed to clarify these complexities.
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页数:29
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