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Iron homeostasis in arthropathies: From pathogenesis to therapeutic potential
Institution:1. State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Medical College of Soochow University, Suzhou, China;2. Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, China;3. Key Laboratory for Space Bioscience and Biotechnology, Institute of Special Environmental Biophysics, School of Life Sciences, Northwestern Polytechnical University, Xi''an, China;4. Research & Development Institute in Shenzhen, Northwestern Polytechnical University, Shenzhen, China;5. Department of Nutrition and Food Hygiene, School of Public Health, Medical College of Soochow University, Suzhou, China;6. Center for Radiological Research, College of Physician and Surgeons, Columbia University, New York, USA
Abstract:Iron is an essential element for proper functioning of cells within mammalian organ systems; in particular, iron homeostasis is critical for joint health. Excess iron can induce oxidative stress damage, associated with the pathogenesis of iron-storage and ageing-related diseases. Therefore, iron levels in body tissues and cells must be tightly regulated. In the past decades, excess iron content within joints has been found in some patients with joint diseases including hemophilic arthropathy, hemochromatosis arthropathy, and osteoarthritis (OA). Currently, increased evidence has shown that iron accumulation is closely associated with multiple pathological changes of these arthropathies. This review summarizes system-level and intracellular regulation of iron homeostasis, and emphasizes the role of iron in synovial alterations, cartilage degeneration, and subchondral bone of several arthropathies. Of note, we discuss the potential link between iron homeostasis and OA pathogenesis. Finally, we discuss the therapeutic potential of maintaining iron homeostasis in these arthropathies.
Keywords:Arthropathy  Osteoarthritis  Chondrocyte  Iron homeostasis  Reactive oxygen species  Ferroptosis
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