Latest Findings on Ferroptosis and Osteoarthropathy

AN Ke; ZHOU Xuedong

doi:10.12182/20231160209

Volume 54 Issue 6

Dec. 2023

Turn off MathJax

Article Contents

Abstract

References

JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES) > 2023 > 54(6): 1294-1299. > DOI: 10.12182/20231160209

AN Ke, ZHOU Xuedong. Latest Findings on Ferroptosis and Osteoarthropathy[J]. Journal of Sichuan University (Medical Sciences), 2023, 54(6): 1294-1299. DOI: 10.12182/20231160209

Citation:

AN Ke, ZHOU Xuedong. Latest Findings on Ferroptosis and Osteoarthropathy[J]. Journal of Sichuan University (Medical Sciences), 2023, 54(6): 1294-1299. DOI: 10.12182/20231160209

Citation:

AN Ke, ZHOU Xuedong. Latest Findings on Ferroptosis and Osteoarthropathy[J]. Journal of Sichuan University (Medical Sciences), 2023, 54(6): 1294-1299. DOI: 10.12182/20231160209

PDF (935 KB)

Latest Findings on Ferroptosis and Osteoarthropathy

AN Ke,
ZHOU Xuedong^,

State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, Department of Cariology and Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China

More Information

Corresponding author:
ZHOU Xuedong, E-mail: zhouxd@scu.edu.cn
Received Date: August 15, 2022
Revised Date: March 20, 2023
Available Online: December 19, 2023
Published Date: December 24, 2023

Abstract

Abstract

Ferroptosis, a newly-discovered mode of programmed cell death, is closely associated with the development of various diseases throughout the human body, such as tumors of the digestive system, ischemia-reperfusion injury, osteoarthropathy, etc. Therefore, ferroptosis has become a hot research topic in many fields of study in recent years, providing new ideas for the prevention and treatment of relevant diseases. Among them, structural lesions in osteoarthropathies involving articular cartilage, subchondral bone, and synovial tissue have been found to be associated with iron overload, as well as oxidative stress, which suggests that inhibition of ferroptosis in relevant joint tissue cells may have a positive effect in halting the development of osteoarthropathy. Herein, focusing on ferroptosis and osteoarthropathy, we summarized the research developments in mechanisms related to iron metabolism and ferroptosis, analyzed the impact of ferroptosis on the pathogenesis and development of osteoarthropathy, and proposed new ideas for medication therapies of osteoarthropathy, taking into account the latest research findings.
- Osteoarthropathy,
- Ferroptosis,
- Iron overload,
- Lipid peroxidation,
- Oxidative stress,
- Review

FullText(HTML)

References (41)

References

[1]	HELMAN S L, ZHOU J, FUQUA B K, et al. The biology of mammalian multi-copper ferroxidases. Biometals,2023,36(2): 263–281. DOI: 10.1007/s10534-022-00370-z
[2]	ANDERSON G J, FRAZER D M. Current understanding of iron homeostasis. Am J Clin Nutr,2017,106(Suppl 6): 1559s–1566s. DOI: 10.3945/ajcn.117.155804
[3]	ASCHEMEYER S, QIAO B, STEFANOVA D, et al. Structure-function analysis of ferroportin defines the binding site and an alternative mechanism of action of hepcidin. Blood,2018,131(8): 899–910. DOI: 10.1182/blood-2017-05-786590
[4]	WANG C Y, BABITT J L. Liver iron sensing and body iron homeostasis. Blood,2019,133(1): 18–29. DOI: 10.1182/blood-2018-06-815894
[5]	SU L J, ZHANG J H, GOMEZ H, et al. Reactive oxygen species-induced lipid peroxidation in apoptosis, autophagy, and ferroptosis. Oxid Med Cell Longev,2019,2019: 5080843. DOI: 10.1155/2019/5080843
[6]	YANG W S, SRIRAMARATNAM R, WELSCH M E, et al. Regulation of ferroptotic cancer cell death by GPX4. Cell,2014,156(1/2): 317–331. DOI: 10.1016/j.cell.2013.12.010
[7]	GAO G, LI J, ZHANG Y, et al. Cellular iron metabolism and regulation. Adv Exp Med Biol,2019,1173: 21–32. DOI: 10.1007/978-981-13-9589-5_2
[8]	HOU W, XIE Y, SONG X, et al. Autophagy promotes ferroptosis by degradation of ferritin. Autophagy,2016,12(8): 1425–1428. DOI: 10.1080/15548627.2016.1187366
[9]	KAGAN V E, MAO G, QU F, et al. Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis. Nat Chem Biol,2017,13(1): 81–90. DOI: 10.1038/nchembio.2238
[10]	CHEN X, LI J, KANG R, et al. Ferroptosis: machinery and regulation. Autophagy,2021,17(9): 2054–2081. DOI: 10.1080/15548627.2020.1810918
[11]	CHU B, KON N, CHEN D, et al. ALOX12 is required for p53-mediated tumour suppression through a distinct ferroptosis pathway. Nat Cell Biol,2019,21(5): 579–591. DOI: 10.1038/s41556-019-0305-6
[12]	HUNTER D J, BIERMA-ZEINSTRA S. Osteoarthritis. Lancet,2019,393(10182): 1745–1759. DOI: 10.1016/s0140-6736(19)30417-9
[13]	SINGH P, MARCU K B, GOLDRING M B, et al. Phenotypic instability of chondrocytes in osteoarthritis: on a path to hypertrophy. Ann N Y Acad Sci,2019,1442(1): 17–34. DOI: 10.1111/nyas.13930
[14]	HSIA A W, EMAMI A J, TARKE F D, et al. Osteophytes and fracture calluses share developmental milestones and are diminished by unloading. J Orthop Res,2018,36(2): 699–710. DOI: 10.1002/jor.23779
[15]	HU Y, CHEN X, WANG S, et al. Subchondral bone microenvironment in osteoarthritis and pain. Bone Res,2021,9(1): 20. DOI: 10.1038/s41413-021-00147-z
[16]	YAO X, SUN K, YU S, et al. Chondrocyte ferroptosis contribute to the progression of osteoarthritis. J Orthop Translat,2021,27: 33–43. DOI: 10.1016/j.jot.2020.09.006
[17]	SIMÃO M, CANCELA M L. Musculoskeletal complications associated with pathological iron toxicity and its molecular mechanisms. Biochem Soc Trans,2021,49(2): 747–759. DOI: 10.1042/bst20200672
[18]	ZHENG L, ZHANG Z, SHENG P, et al. The role of metabolism in chondrocyte dysfunction and the progression of osteoarthritis. Ageing Res Rev,2021,66: 101249. DOI: 10.1016/j.arr.2020.101249
[19]	SUN K, GUO Z, HOU L C, et al. Iron homeostasis in arthropathies: From pathogenesis to therapeutic potential. Ageing Res Rev,2021,72: 101481. DOI: 10.1016/j.arr.2021.101481
[20]	PAN Z, HE Q, ZENG J, et al. Naringenin protects against iron overload-induced osteoarthritis by suppressing oxidative stress. Phytomedicine,2022,105: 154330. DOI: 10.1016/j.phymed.2022.154330
[21]	LIU F, ZHANG W L, MENG H Z, et al. Regulation of DMT1 on autophagy and apoptosis in osteoblast. Int J Med Sci,2017,14(3): 275–283. DOI: 10.7150/ijms.17860
[22]	ISHII K A, FUMOTO T, IWAI K, et al. Coordination of PGC-1beta and iron uptake in mitochondrial biogenesis and osteoclast activation. Nat Med,2009,15(3): 259–266. DOI: 10.1038/nm.1910
[23]	YANG J, DONG D, LUO X, et al. Iron overload-induced osteocyte apoptosis stimulates osteoclast differentiation through increasing osteocytic rankl productionin vitro. Calcif Tissue Int,2020,107(5): 499–509. DOI: 10.1007/s00223-020-00735-x
[24]	SELLAM J, BERENBAUM F. The role of synovitis in pathophysiology and clinical symptoms of osteoarthritis. Nat Rev Rheumatol,2010,6(11): 625–635. DOI: 10.1038/nrrheum.2010.159
[25]	YAZAR M, SARBAN S, KOCYIGIT A, et al. Synovial fluid and plasma selenium, copper, zinc, and iron concentrations in patients with rheumatoid arthritis and osteoarthritis. Biol Trace Elem Res,2005,106(2): 123–132. DOI: 10.1385/bter:106:2:123
[26]	NIEUWENHUIZEN L, SCHUTGENS R E, Van ASBECK B S, et al. Identification and expression of iron regulators in human synovium: evidence for upregulation in haemophilic arthropathy compared to rheumatoid arthritis, osteoarthritis, and healthy controls. Haemophilia,2013,19(4): e218–227. DOI: 10.1111/hae.12208
[27]	HAKOBYAN N, KAZARIAN T, JABBAR A A, et al. Pathobiology of hemophilic synovitis I: overexpression of mdm2 oncogene. Blood,2004,104(7): 2060–2064. DOI: 10.1182/blood-2003-12-4231
[28]	WU C L, HARASYMOWICZ N S, KLIMAK M A, et al. The role of macrophages in osteoarthritis and cartilage repair. Osteoarthritis Cartilage,2020,28(5): 544–554. DOI: 10.1016/j.joca.2019.12.007
[29]	ZHOU Y, QUE K T, ZHANG Z, et al. Iron overloaded polarizes macrophage to proinflammation phenotype through ROS/acetyl-p53 pathway. Cancer Med,2018,7(8): 4012–4022. DOI: 10.1002/cam4.1670
[30]	Di MAGGIO R, MAGGIO A. The new era of chelation treatments: effectiveness and safety of 10 different regimens for controlling iron overloading in thalassaemia major. Br J Haematol,2017,178(5): 676–688. DOI: 10.1111/bjh.14712
[31]	RODRIGUES DEMORAIS T, GAMBERO A. Iron chelators in obesity therapy--old drugs from a new perspective? Eur J Pharmacol,2019,861: 172614. DOI: 10.1016/j.ejphar.2019.172614
[32]	TCHETINA E V, MARKOVA G A, POOLE A R, et al. Deferoxamine suppresses collagen cleavage and protease, cytokine, and COL10A1 expression and upregulates AMPK and Krebs cycle genes in human osteoarthritic cartilage. Eur J Pharmacol,2016,2016: 6432867. DOI: 10.1155/2016/6432867
[33]	KALANAKY S, HAFIZI M, SAFARI S, et al. TLc-A, the leading nanochelating-based nanochelator, reduces iron overloadin vitro and in vivo. Int J Hematol,2016,103(3): 274–282. DOI: 10.1007/s12185-015-1932-8
[34]	YU L, HE M, LIU S, et al. Fluorescent egg white-based carbon dots as a high-sensitivity iron chelator for the therapy of nonalcoholic fatty liver disease by iron overload in zebrafish. ACS Appl Mater Interfaces,2021,13(46): 54677–54689. DOI: 10.1021/acsami.1c14674
[35]	ZUO S, ZOU W, WU R M, et al. Icariin alleviates IL-1β-induced matrix degradation by activating the NRF2/ARE pathway in human chondrocytes. Drug Des Devel Ther,2019,13: 3949–3961. DOI: 10.2147/dddt.S203094
[36]	ZHAO L, WANG Y, WANG Z, et al. Effects of dietary resveratrol on excess-iron-induced bone loss via antioxidative character. J Nutr Biochem,2015,26(11): 1174–1182. DOI: 10.1016/j.jnutbio.2015.05.009
[37]	TIAN Q, WU S, DAI Z, et al. Iron overload induced death of osteoblasts in vitro: involvement of the mitochondrial apoptotic pathway. Peer J,2016,4: e2611. DOI: 10.7717/peerj.2611
[38]	SHEN C L, CHYU M C, WANG J S. Tea and bone health: steps forward in translational nutrition. Am J Clin Nutr,2013,98(6 Suppl): 1694s–1699s. DOI: 10.3945/ajcn.113.058255
[39]	WU D Q, ZHONG H M, DING Q H, et al. Protective effects of biochanin A on articular cartilage: in vitro and in vivo studies. BMC Complement Altern Med,2014,14: 444. DOI: 10.1186/1472-6882-14-444
[40]	XU Z, SUN W, LI Y, et al. The regulation of iron metabolism by hepcidin contributes to unloading-induced bone loss. Bone,2017,94: 152–161. DOI: 10.1016/j.bone.2016.09.023
[41]	O'NEILL T, FELSON D. Mechanisms of osteoarthritis (OA) pain. Curr Osteoporos Rep,2018,16(5): 611–616. DOI: 10.1007/s11914-018-0477-1

OPEN ACCESS This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International license (CC BY-NC 4.0). In other words, the full-text content of the journal is made freely available for third-party users to copy and redistribute in any medium or format, and to remix, transform, and build upon the content of the journal. You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may not use the content of the journal for commercial purposes. For more information about the license, visit https://creativecommons.org/licenses/by-nc/4.0

Relative Articles

[1]	CHEN Xiunan, WANG Ruiqi, SHAN Hongying, ZHOU Ping, LI Rong. Quercetin Alleviates H₂O₂-Induced Oxidative Stress Damage to Human Endometrial Stromal Cells by Inhibiting the p38 MAPK/NOX4 Signaling Pathway[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2024, 55(3): 552-558. DOI: 10.12182/20240560107
[2]	GONG Xue, HUANG Jin, WANG Chichiu. Research Progress in the Role of Mitochondrial Dysfunction in Endometriosis-Associated Infertility[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2024, 55(3): 521-526. DOI: 10.12182/20240560404
[3]	ZHOU Hao, CHEN Tao, WU Aimin. Effects of Oxidative Stress on Mitochondrial Functions and Intervertebral Disc Cells[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2024, 55(2): 249-255. DOI: 10.12182/20240360201
[4]	YI Xiangling, HE Yani, CHEN Kehong. Research Progress in Stress-Induced Senescence of Renal Tubular Cells in Diabetic Nephropathy[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2023, 54(6): 1085-1090. DOI: 10.12182/20231160107
[5]	FANG Chenxi, SUN Liya, LIU Yan, XIAO Li, SUN Lin. Non-Classical Clinical Types and Pathological Changes of Diabetic Kidney Disease: A Review[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2023, 54(6): 1074-1079. DOI: 10.12182/20231160102
[6]	LIU Ying, PENG Wei, QI Hong-bo. Glucose Metabolism-Derived Nicotinamide Adenine Dinucleotide Phosphate in Late-Onset Preeclampsia Placenta Tissue and Its Correlation with Oxidative Stress[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2022, 53(6): 1028-1032. DOI: 10.12182/20221160212
[7]	OU Wei, LIANG Yu, QING Yu, DENG Yan, WU Wei, LI Tao. The Effect of Short-Term Intermittent Hypoxia Exposure on Mouse Myocardial Oxidative Stress and Cardiac Function[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2022, 53(1): 98-104. DOI: 10.12182/20220160103
[8]	JI Li-wei, DENG Yan, LI Tao. Effect of Ketone Body β-Hydroxybutyrate to Attenuate Inflammation-Induced Mitochondrial Oxidative Stress in Vascular Endothelial Cells[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2021, 52(6): 954-959. DOI: 10.12182/20211160202
[9]	FENG Xiao-rong, YAO Jie, WU Ya, CHENG Xia, ZOU Ping-jin, WANG Hua, YANG Mu. Research and Application of Stem Cell-Based Therapy in Idiopathic Pulmonary Fibrosis: A Review[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2021, 52(3): 373-379. DOI: 10.12182/20210560304
[10]	WANG Kui, MING Hui, ZUO Jing, TIAN Hai-long, HUANG Can-hua. A Review of the Redox Regulation of Tumor Metabolism[J]. JOURNAL OF SICHUAN UNIVERSITY (MEDICAL SCIENCES), 2021, 52(1): 57-63. DOI: 10.12182/20210160204

Supplements (0)

Cited By

Cited by

Periodical cited type(2)

1.	王成毅，蔡粤芳，宁振求，邓敏贞，孙景波，Sookja Kim CHUNG，李岩，程骁. 壮通饮通过Nrf2-SCL7A11/xCT-Gpx4通路调控铁死亡改善脑缺血再灌注损伤. 中山大学学报(医学科学版). 2024(04): 539-548 .
2.	董逸波，唐锐，杨涵翔，樊效鸿，余洋. 独活寄生汤抑制铁死亡治疗膝骨关节炎研究进展. 辽宁中医药大学学报. 2024(12): 76-81 .

Other cited types(1)

Get Citation

PDF

XML

Article views (311) PDF downloads (40) Cited by(3)

Latest Findings on Ferroptosis and Osteoarthropathy