细胞死亡在骨关节炎中的研究进展
Research Advances in Cell Death in Osteoarthritis
DOI: 10.12677/ACM.2023.133639, PDF,    国家自然科学基金支持
作者: 翟传兴, 赵 晟, 张泽浩, 孙兆丰:单位济宁医学院临床医学院,山东 济宁;王国栋, 张元民*:济宁医学院附属医院关节与运动医学科,山东 济宁
关键词: 细胞焦亡细胞凋亡铁死亡骨关节炎Pyroptosis Apoptosis Ferroptosis Osteoarthritis
摘要: 新的研究表明,骨关节炎(osteoarthritis, OA)的发展与预后可以受到各种细胞死亡的机制和细胞因子类型的调控。因此,为了更好地了解OA的发病机制和其进展,为此本文阐述了各种细胞因子、细胞死亡的过程和OA之间的作用机制,本文阐述了细胞焦亡、铁死亡(ferroptosis)和细胞凋亡的细胞形态特征和分子机制,并回顾了近年来有关细胞死亡在OA中的作用机制的相关报道和研究。
Abstract: New research suggests that the development and prognosis of osteoarthritis can be regulated by various mechanisms of cell death and cytokine types. Therefore, in order to better understand the pathogenesis and progression of osteoarthritis, this paper elaborates the mechanism between var-ious cytokines, the process of cell death and osteoarthritis, the cell morphological characteristics and molecular mechanisms of pyrozowhosis, ferrosis and apoptosis, and reviews the relevant re-ports and studies on the mechanism of cell death in osteoarthritis in recent years.
文章引用:翟传兴, 赵晟, 张泽浩, 孙兆丰, 王国栋, 张元民. 细胞死亡在骨关节炎中的研究进展[J]. 临床医学进展, 2023, 13(3): 4454-4458. https://doi.org/10.12677/ACM.2023.133639

参考文献

[1] Jorgensen, I., Rayamajhi, M. and Miao, E.A. (2017) Programmed Cell Death as a Defence against Infection. Nature Re-views Immunology, 17, 151-164. [Google Scholar] [CrossRef] [PubMed]
[2] Fuchs, Y. and Steller, H. (2011) Pro-grammed Cell Death in Animal Development and Disease. Cell, 147, 742-758. [Google Scholar] [CrossRef] [PubMed]
[3] Majno, G. and Joris, I. (1995) Apoptosis, Oncosis, and Necrosis. An Overview of Cell Death. The American Journal of Pathology, 146, 3-15.
[4] Dixon, S.J., et al. (2012) Ferroptosis: An Iron-Dependent form of Nonapoptotic Cell Death. Cell, 149, 1060-1072. [Google Scholar] [CrossRef] [PubMed]
[5] Dixon, S.J. and Stockwell, B.R. (2014) The Role of Iron and Reac-tive Oxygen Species in Cell Death. Nature Chemical Biology, 10, 9-17. [Google Scholar] [CrossRef] [PubMed]
[6] Zhou, H., et al. (2016) IRAKM-Mincle Axis Links Cell Death to In-flammation: Pathophysiological Implications for Chronic Alcoholic Liver Disease. Hepatology, 64, 1978-1993. [Google Scholar] [CrossRef] [PubMed]
[7] Hosseinzadeh, A., et al. (2016) Apoptosis Signaling Pathways in Osteoar-thritis and Possible Protective Role of Melatonin. Journal of Pineal Research, 61, 411-425. [Google Scholar] [CrossRef] [PubMed]
[8] Martel-Pelletier, J., et al. (2016) Osteoarthritis. Nature Reviews Disease Primers, 2, 16072. [Google Scholar] [CrossRef] [PubMed]
[9] Koelling, S., et al. (2009) Migratory Chondrogenic Progenitor Cells from Repair Tissue during the Later Stages of Human Osteoarthritis. Cell Stem Cell, 4, 324-335. [Google Scholar] [CrossRef] [PubMed]
[10] Sanchez, C., et al. (2012) Regulation of Subchondral Bone Osteo-blast Metabolism by Cyclic Compression. Arthritis & Rheumatology, 64, 1193-1203. [Google Scholar] [CrossRef] [PubMed]
[11] An, S., et al. (2020) Pyroptosis Plays a Role in Osteoarthritis. Aging and Disease, 11, 1146-1157. [Google Scholar] [CrossRef
[12] Liu, G., et al. (2020) USP7 Inhibition Alleviates H(2)O(2)-Induced Injury in Chondrocytes via Inhibiting NOX4/NLRP3 Pathway. Frontiers in Pharmacology, 11, Article ID: 617270. [Google Scholar] [CrossRef] [PubMed]
[13] Zychlinsky, A., Prevost, M.C. and Sansonetti, P.J. (1992) Shigella flexneri Induces Apoptosis in Infected Macrophages. Nature, 358, 167-169. [Google Scholar] [CrossRef] [PubMed]
[14] Man, S.M. and Kanneganti, T.D. (2015) Regulation of Inflammasome Acti-vation. Immunological Reviews, 265, 6-21. [Google Scholar] [CrossRef] [PubMed]
[15] Wang, S., et al. (2021) Exogenous Stromal Cell-Derived Factor-1 (SDF-1) Suppresses the NLRP3 Inflammasome and Inhibits Pyroptosis in Synoviocytes from Osteoarthritic Joints via Activation of the AMPK Signaling Pathway. Inflammopharmacology, 29, 695-704. [Google Scholar] [CrossRef] [PubMed]
[16] Bartlett, R., Stokes, L. and Sluyter, R. (2014) The P2X7 Recep-tor Channel: Recent Developments and the Use of P2X7 Antagonists in Models of Disease. Pharmacological Reviews, 66, 638-675. [Google Scholar] [CrossRef] [PubMed]
[17] Li, Z., et al. (2021) P2X7 Receptor Induces Pyroptotic In-flammation and Cartilage Degradation in Osteoarthritis via NF-kappaB/NLRP3 Crosstalk. Oxidative Medicine and Cel-lular Longevity, 2021, Article ID: 8868361. [Google Scholar] [CrossRef] [PubMed]
[18] Yu, H., et al. (2021) Morroniside Attenuates Apoptosis and Pyroptosis of Chondrocytes and Ameliorates Osteoarthritic Development by Inhibiting NF-kappaB Signaling. Journal of Eth-nopharmacology, 266, Article ID: 113447. [Google Scholar] [CrossRef] [PubMed]
[19] Yan, Z., et al. (2020) Activating Nrf2 Signalling Alleviates Osteo-arthritis Development by Inhibiting Inflammasome Activation. Journal of Cellular and Molecular Medicine, 24, 13046-13057. [Google Scholar] [CrossRef] [PubMed]
[20] Stockwell, B.R., et al. (2017) Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. Cell, 171, 273-285. [Google Scholar] [CrossRef] [PubMed]
[21] Fang, X., et al. (2020) Loss of Cardiac Ferritin H Facilitates Cardi-omyopathy via Slc7a11-Mediated Ferroptosis. Circulation Research, 127, 486-501. [Google Scholar] [CrossRef
[22] Yu, Y., et al. (2020) Hepatic Transferrin Plays a Role in Systemic Iron Homeostasis and Liver Ferroptosis. Blood, 136, 726-739. [Google Scholar] [CrossRef] [PubMed]
[23] Stockwell, B.R., Jiang, X. and Gu, W. (2020) Emerging Mecha-nisms and Disease Relevance of Ferroptosis. Trends in Cell Biology, 30, 478-490. [Google Scholar] [CrossRef] [PubMed]
[24] Urano, S., et al. (2016) Iron Depletion Enhances the Effect of So-rafenib in Hepatocarcinoma. Cancer Biology & Therapy, 17, 648-656. [Google Scholar] [CrossRef] [PubMed]
[25] Yao, X., et al. (2021) Chondrocyte Ferroptosis Contribute to the Progression of Osteoarthritis. The Journal of Orthopaedic Translation, 27, 33-43. [Google Scholar] [CrossRef] [PubMed]
[26] Luo, H. and Zhang, R. (2021) Icariin Enhances Cell Survival in Lip-opolysaccharide-Induced Synoviocytes by Suppressing Ferroptosis via the Xc-/GPX4 Axis. Experimental and Thera-peutic Medicine, 21, 72. [Google Scholar] [CrossRef] [PubMed]
[27] Luke, J.J., Van De Wetering, C.I. and Knudson, C.M. (2003) Lym-phoma Development in Bax Transgenic Mice Is Inhibited by Bcl-2 and Associated with Chromosomal Instability. Cell Death & Differentiation, 10, 740-748. [Google Scholar] [CrossRef] [PubMed]
[28] Jorgensen, A., Kjaer, M. and Heinemeier, K.M. (2017) The Effect of Aging and Mechanical Loading on the Metabolism of Articular Cartilage. The Journal of Rheumatology, 44, 410-417. [Google Scholar] [CrossRef] [PubMed]
[29] Lu, R., et al. (2023) Mulberroside A Alleviates Osteoarthritis via Re-storing Impaired Autophagy and Suppressing MAPK/NF-kappaB/PI3K-AKT-mTOR Signaling Pathways. iScience, 26, Article ID: 105936. [Google Scholar] [CrossRef] [PubMed]
[30] Latourte, A., Kloppenburg, M. and Richette, P. (2020) Emerging Pharmaceutical Therapies for Osteoarthritis. Nature Reviews Rheumatology, 16, 673-688. [Google Scholar] [CrossRef] [PubMed]
[31] Chevalier, X., Conrozier, T. and Richette, P. (2011) Desperately Looking for the Right Target in Osteoarthritis: The Anti-IL-1 Strategy. Arthritis Research & Therapy, 13, 124. [Google Scholar] [CrossRef] [PubMed]
[32] Qin, J., et al. (2013) Response to “TNF/TNFR Signal Transduction Path-way-Mediated Anti-Apoptosis and Anti-Inflammatory Effects of Sodium Ferulate on IL-1beta-Induced Rat Osteoarthritis Chondrocytes in Vitro”—Authors’ Reply. Arthritis Research & Therapy, 15, 409. [Google Scholar] [CrossRef] [PubMed]
[33] Lu, G., et al. (2020) LINC00623/miR-101/HRAS Axis Modulates IL-1beta-Mediated ECM Degradation, Apoptosis and Senescence of Osteoarthritis Chondrocytes. Aging (Albany NY), 12, 3218-3237. [Google Scholar] [CrossRef] [PubMed]
[34] Cai, C., et al. (2019) MiR-27a Promotes the Autophagy and Apoptosis of IL-1beta Treated-Articular Chondrocytes in Osteoarthritis through PI3K/AKT/mTOR Signaling. Aging (Albany NY), 11, 6371-6384. [Google Scholar] [CrossRef] [PubMed]
[35] Shajahan, A.N., et al. (2012) Tyrosine-Phosphorylated Caveolin-1 (Tyr-14) Increases Sensitivity to Paclitaxel by Inhibiting BCL2 and BCLxL Proteins via c-Jun N-Terminal Kinase (JNK). Journal of Biological Chemistry, 287, 17682-17692. [Google Scholar] [CrossRef