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Role of proinflammatory cytokines in the pathophysiology of osteoarthritis
Abstract
Osteoarthritis (OA) is associated with cartilage destruction, subchondral bone remodeling and inflammation of the synovial membrane, although the etiology and pathogenesis underlying this debilitating disease are poorly understood. Secreted inflammatory molecules, such as proinflammatory cytokines, are among the critical mediators of the disturbed processes implicated in OA pathophysiology. Interleukin (IL)-1β and tumor necrosis factor (TNF), in particular, control the degeneration of articular cartilage matrix, which makes them prime targets for therapeutic strategies. Animal studies provide support for this approach, although only a few clinical studies have investigated the efficacy of blocking these proinflammatory cytokines in the treatment of OA. Apart from IL-1β and TNF, several other cytokines including IL-6, IL-15, IL-17, IL-18, IL-21, leukemia inhibitory factor and IL-8 (a chemokine) have also been shown to be implicated in OA and could possibly be targeted therapeutically. This Review discusses the current knowledge regarding the role of proinflammatory cytokines in the pathophysiology of OA and addresses the potential of anticytokine therapy in the treatment of this disease.
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“Because TNF-α signaling primarily via TNFR1 binds TRADD and RIPK1 to generate complexes that activate NF-κB, MAPKs, and caspases, IL-1β and TNF-α cooperate to enhance chronic inflammation in degenerative joint disease [42,43].”
From Biomarker-Guided Imaging and AI-Augmented Diagnosis of Degenerative Joint Disease (2025) · cites this paper as [42]
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Jenei-Lanzl, Z., Maurer, S., Brenner, R. E., Zaucke, F., Fuchs, M., & Riegger, J. (2025) · Archives of pharmacal research · doi:10.1007/s12272-025-01551-3 · Cited by 35
“However, in the phase 2 clinical study, which included 170 subjects (160 completed the study, ≥ 18 years, exclusion criteria: secondary OA and KL grade 4) no significant differences were identified for 50 mg or 150 mg Anakinra® in the WOMAC pain, function and stiffness score (week 4) compared to the placebo group.”
InfluentialLiu, X., Li, Y., Zhao, J., Hu, Z., Fang, W., Ke, J., Li, W., & Long, X. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.110781 · Cited by 39
The potential remedy of melatonin on osteoarthritis
Lu, K.-H., Lu, P. W., Lu, E. W.-H., Tang, C.-H., Su, S.-C., Lin, C.-W., & Yang, S.-F. (2021) · Journal of Pineal Research · doi:10.1111/jpi.12762 · Cited by 35
Sun, Y.-Q., Huang, K., Mo, L.-H., Ahmad, A., Wang, D., Rong, Z.-J., Peng, H., Cai, H.-H., & Liu, G. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.730557 · Cited by 35
“Studies have shown that the cytokine IL-6, IL-1β and IL-18 can promote inflammation and apoptosis of chondrocytes, they inhibit the expression of aggrecan and stimulate the expression of MMPs, thus contribute to the pathogenesis of OA (Bao et al., 2020; Kapoor et al., 2011).”
BackgroundLin, Z., Miao, J., Zhang, T., He, M., Zhou, X.-N., Zhang, H., Gao, Y., & Bai, L. (2021) · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · doi:10.1016/j.biopha.2020.111199 · Cited by 35
Wang, B., Shao, Z., Gu, M., Ni, L., Shi, Y.-F., Yan, Y.-Z., Wu, A., Jin, H., Chen, J.-X., Pan, X., et al. (2020) · Journal of Cellular Physiology · doi:10.1002/jcp.30154 · Cited by 35
Mengsteab, P. Y., Otsuka, T., McClinton, A., Shemshaki, N. S., Shah, S., Kan, H. M., Obopilwe, E., Vella, A., Nair, L., & Laurencin, C. (2020) · Proceedings of the National Academy of Sciences of the United States of America · doi:10.1073/pnas.2012347117 · Cited by 35
Role of mitochondria in mediating chondrocyte response to mechanical stimuli
He, Y., Makarczyk, M. J., & Lin, H. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.118602 · Cited by 36
Wang, Q., Zhuang, D., Feng, W.-C., Ma, B.-T., Qin, L., & Jin, L.-L. (2020) · Saudi Pharmaceutical Journal · doi:10.1016/j.jsps.2020.09.016 · Cited by 35
Xu, J., Qian, X.-Z., & Ding, R. (2020) · Journal of Orthopaedic Surgery and Research · doi:10.1186/s13018-021-02378-6 · Cited by 35
Jia, Y., He, W., Zhang, H., He, L., Wang, Y., Zhang, T., Peng, J.-X., Sun, P., & Qian, Y. (2020) · Drug Design, Development and Therapy · doi:10.2147/dddt.s244462 · Cited by 35
Singh, M., Mastana, S. S., Singh, S., Juneja, P. K., Kaur, T., & Singh, P. (2020) · Cytokine · doi:10.1016/j.cyto.2020.154985 · Cited by 40
Lei, J.-L., Fu, Y.-H., Zhuang, Y., Zhang, K., & Lu, D.-G. (2019) · Journal of Cellular Physiology · doi:10.1002/jcp.28882 · Cited by 35
Alleviation of Murine Osteoarthritis by Cartilage‐Specific Deletion of IκBζ
Choi, M.-C., Maruyama, T., Chun, C.-H., & Park, Y. (2018) · Arthritis & Rheumatology · doi:10.1002/art.40514 · Cited by 35
“To explore the possible role of IjBf in OA cartilage destruction, we first examined expression levels of IjBf in mouse chondrocytes stimulated with IL-1b, a proinflammatory cytokine associated with OA pathogenesis (6).”
Sun, J., Wei, X., Wang, Z., Liu, Y., Lu, J., Lu, Y., Cui, M., Zhang, X., & Li, F. (2017) · Journal of Cellular Biochemistry · doi:10.1002/jcb.26470 · Cited by 34
“OA is not a single disease but rather a convergent joint failure, triggered and maintained by numerous stimuli, including biochemical, inflammatory or genetic factors.(30) We found that IL-1β and TNF-α could induce the expressions of Sema3A and Nrp1 in chondrocytes in vitro, suggesting the upregulated expressions of S…”
BackgroundThe protective effect of phloretin in osteoarthritis: an in vitro and in vivo study.
Zheng, W., Chen, C., Zhang, C., Cai, L., & Chen, H. (2018) · Food & Function · doi:10.1039/c7fo01199g · Cited by 35
Metabolic Responses of Meniscus to IL-1β
Cook, A., Cook, J., & Stoker, A. (2018) · The journal of knee surgery · doi:10.1055/s-0037-1615821 · Cited by 35
Peat, F. J., Colbath, A. C., Bentsen, L. M., Goodrich, L., & King, M. (2017) · Photomedicine and Laser Surgery · doi:10.1089/pho.2017.4344 · Cited by 35
Li, C.-W., Chen, K., Kang, H., Yan, Y.-F., Liu, K., Guo, C.-J., Qi, J., Yang, K., Wang, F., Guo, L., et al. (2017) · Cell Death and Disease · doi:10.1038/cddis.2017.534 · Cited by 35
Ding, L., Hong, X.-P., Sun, B.-D., Huang, Q., Wang, X., Liu, X., Li, L., Huang, Z., & Liu, D.-Z. (2017) · Scientific Reports · doi:10.1038/s41598-017-11397-5 · Cited by 35
Discovery of circulating proteins associated to knee radiographic osteoarthritis
Lourido, L., Ayoglu, B., Fernández-Tajes, J., Oreiro, N., Henjes, F., Hellström, C., Schwenk, J., Ruiz-Romero, C., Nilsson, P., & Blanco, F. (2017) · Scientific Reports · doi:10.1038/s41598-017-00195-8 · Cited by 35
Bone morphogenetic protein-2 provokes interleukin-18-induced human intervertebral disc degeneration
Ye, S., Ju, B., Wang, H., & Lee, K. (2016) · Bone & Joint Research · doi:10.1302/2046-3758.59.bjr-2016-0032.r1 · Cited by 35
Chen, Q., Mei, X.-F., Han, G., Ling, P.-X., Guo, B., Guo, Y., Shao, H.-R., Wang, G., Cui, Z., Bai, Y., et al. (2015) · Carbohydrate Polymers · doi:10.1016/j.carbpol.2015.06.004 · Cited by 35
“…apoptosis pathways; (2) disrupting cartilage-specific xtracellular matrix (ECM) homeostasis by inhibiting the synthesis f type II collagen and proteoglycans; and (3) upregulating matrix etalloproteinases, with subsequent degradation of the cartilage atrix (Kapoor et al., 2011; Kim et al., 2002).”
BackgroundDing, X., Zhang, Y.-J., Huang, Y., Liu, S., Lu, H., & Sun, T.-Z. (2015) · International Immunopharmacology · doi:10.1016/j.intimp.2015.03.024 · Cited by 35
Enhancing inflammatory and chemotactic signals to regulate bone regeneration.
Czekanska, E. M., Ralphs, J., Alini, M., & Stoddart, M. (2014) · European Cells & Materials · doi:10.22203/ecm.v028a22 · Cited by 35
Muñóz-Valle, J., Oregón-Romero, E., Rangel-Villalobos, H., Martínez-Bonilla, G., Castañeda-Saucedo, E., Salgado-Goytia, L., Leyva-Vázquez, M., Illades-Aguiar, B., Alarcón-Romero, L. D. C., Espinoza-Rojo, M., et al. (2014) · Clinical and Experimental Medicine (Testo stampato) · doi:10.1007/s10238-012-0216-3 · Cited by 35
“In OA patients, TNFa levels are elevated in the synovial fluid, synovial membrane, subchondral bone and cartilage [2].”
BackgroundLandman, E., Miclea, R., van Blitterswijk, C. V., & Karperien, M. (2013) · Arthritis Research & Therapy · doi:10.1186/ar4273 · Cited by 35
“Introduction In degenerative cartilage diseases such as osteoarthritis (OA) and rheumatoid arthritis (RA), the balance between anabolic and catabolic processes is shifted toward breakdown of the extracellular cartilage matrix [1-3].”
Ex vivo effect of gold nanoparticles on porcine synovial membrane
Labens, R., Lascelles, B., Charlton, A. N., Ferrero, N. R., van Wettere, A. V., Xia, X. R., & Blikslager, A. (2013) · Tissue Barriers · doi:10.4161/tisb.24314 · Cited by 35
Wang, J.-H., Shih, K.-S., Liou, J., Wu, Y.-W., Chang, A. S.-Y., Wang, K., Tsai, C.-L., & Yang, C.-R. (2012) · PLoS ONE · doi:10.1371/journal.pone.0031368 · Cited by 35
“works formation, cartilage catabolism elevation and anabolism suppression [2].”
Azim, S., Nicholson, J., Rebecchi, M., Galbavy, W., Feng, T., Rizwan, S., Reinsel, R., Kaczocha, M., & Benveniste, H. (2018) · Knee (Oxford) · doi:10.1016/j.knee.2017.12.001 · Cited by 35
Li, M., Jia, X., Lai, P., Ma, Y., Li, F., Yang, L., Zhang, S., Yang, C., Luo, Y., & Wang, Q. (2025) · Journal of Controlled Release · doi:10.1016/j.jconrel.2025.114039 · Cited by 28
5-aminosalicylic acid suppresses osteoarthritis through the OSCAR-PPARγ axis
Kim, J., Ryu, G., Seo, J., Go, M., Kim, G., Yi, S., Kim, S., Lee, H., Lee, J., Kim, H. S., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-45174-6 · Cited by 43
Sun, W.-X., Qu, S., Ji, M.-X., Sun, Y.-L., & Hu, B.-Q. (2023) · Heliyon · doi:10.1016/j.heliyon.2023.e19934 · Cited by 34
“Osteoarthritis (OA), the most common chronic osteoarthropathy around the world, is mainly characterized by progressive degradation of articular cartilage, synovial tissue inflammation, subchondral bone remodeling and osteophyte formation [1,2].”
BackgroundIntra-Articular Collagen Injections for Osteoarthritis: A Narrative Review
Tarantino, D., Mottola, R., Palermi, S., Sirico, F., Corrado, B., & Gnasso, R. (2023) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph20054390 · Cited by 34
“Pro-inflammatory factors such as TNF-β, IL-6, IL-1α, and IL-1β are released, stimulating cartilage-degrading enzymes such as a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), and matrix metalloproteinases (MMPs) [22].”
BackgroundKrawetz, R., Wu, Y. E., Bertram, K., Shonak, A., Masson, A., Ren, G., Leonard, C., Kapoor, M., Matyas, J., & Salo, P. (2022) · Cell Death and Disease · doi:10.1038/s41419-022-04919-1 · Cited by 34
“INTRODUCTION Osteoarthritis (OA) is characterized by a persistent homeostatic imbalance, with catabolism outpacing anabolism, which accompanies articular cartilage degeneration, joint pain, and disability [1, 2].”
BackgroundSelf-citationPferdehirt, L., Damato, A. R., Dudek, M., Meng, Q.-J., Herzog, E., & Guilak, F. (2022) · Science Advances · doi:10.1126/sciadv.abj8892 · Cited by 34
Pei, W.-B., Huang, X.-J., Ni, B., Zhang, R., Niu, G., & You, H.-B. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.730312 · Cited by 34
“IL-1β induces the expression of pro-inflammatory factors, including iNOS, COX2, MMPs and ADAMTS5.”
BackgroundInfluentialDravid, A. A., Dhanabalan, K. M., Agarwal, S., & Agarwal, R. (2021) · Bioengineering & Translational Medicine · doi:10.1002/btm2.10281 · Cited by 44
“production of catabolic enzymes.(10) This chronic, low-grade inflammation is a significant driver of OA and is reflected in the surge in the levels of inflammatory cytokines in the synovial fluid and systemic circulation.”
BackgroundInvolvement of Macrophages and Spinal Microglia in Osteoarthritis Pain
Pan, T., Pan, F., Gao, W., Hu, S.-S., & Wang, D. (2021) · Current Rheumatology Reports · doi:10.1007/s11926-021-00997-w · Cited by 34
Kadir, N. D., Yang, Z., Hassan, A., Denslin, V., & Lee, E. H. (2021) · Stem cell research & therapeutics · doi:10.1186/s13287-021-02137-8 · Cited by 34
“Following cartilage injury or in osteoarthritis, degenerative, and apoptotic joint environment are perpetuated as the heightened level of pro-inflammatory cytokines and catabolic factors suppressed the chondrocyte anabolic activities [52].”
BackgroundBao, J.-P., Yan, W., Xu, K., Chen, M.-Y., Chen, Z., Ran, J.-S., Xiong, Y., Wu, L.-D., & Seth, R. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/7517219 · Cited by 34
“Furthermore, in OA synovitis, FLS adhere to chondrocytes and the latter secrete inflammation mediators and activate MMPs, resulting in the acceleration of OA progression [9, 10].”
BackgroundChen, H., & Chen, L.-B. (2020) · Bone & Joint Research · doi:10.1302/2046-3758.93.bjr-2019-0140.r2 · Cited by 34
Lee, Y.-M., Son, E., Kim, S.-H., & Kim, D.-S. (2019) · Phytomedicine · doi:10.1016/j.phymed.2019.153095 · Cited by 34
CCL2 But Not CCR2 Is Required for Spontaneous Articular Cartilage Regeneration Post‐Injury
Jablonski, C., Leonard, C., Salo, P., & Krawetz, R. (2019) · Journal of Orthopaedic Research · doi:10.1002/jor.24444 · Cited by 34
Active viscosupplements for osteoarthritis treatment.
Pontes-Quero, G. M., García-Fernández, L., Aguilar, M., Román, J. S., Pérez-Cano, J. P., & Vázquez-Lasa, B. (2019) · Seminars in Arthritis & Rheumatism · doi:10.1016/j.semarthrit.2019.02.008 · Cited by 34
Wang, Z.-W., Chen, L., Hao, X.-R., Qu, Z.-N., Huang, S.-B., Ma, X.-J., Wang, J.-C., & Wang, W.-M. (2019) · World Journal of Clinical Cases · doi:10.12998/wjcc.v7.i11.1262 · Cited by 34
Protein Cytl1: its role in chondrogenesis, cartilage homeostasis, and disease
Zhu, S.-P., Kuek, V., Bennett, S., Xu, H.-Z., Rosen, V., & Xu, J.-K. (2019) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-019-03137-x · Cited by 34
MiR-146b accelerates osteoarthritis progression by targeting alpha-2-macroglobulin
Liu, X., Liu, L.-L., Zhang, H.-B., Shao, Y., Chen, Z., Feng, X., Fang, H., Zhao, C., Pan, J.-Y., Zhang, H.-Y., et al. (2019) · Aging · doi:10.18632/aging.102160 · Cited by 34
“Treatment of IL-1β stimulated the ECM-degrading enzyme syntheses and secretion, leading to the chondrocyte ECM breakdown and OA development [22], while suppression of IL-1β-induced inflammatory factors with neutralizing antibodies or small molecular inhibitors was able to prevent and treat OA [23, 24].”
BackgroundPark, H.-M., Kwon, Y.-J., Kim, H.-S., & Lee, Y.-J. (2019) · Journal of Clinical Medicine · doi:10.3390/jcm8030356 · Cited by 34
“Pro-inflammatory cytokines such as IL-6 and TNF-α levels are elevated in the synovial fluid and cartilage of patients with osteoarthritis and chronic elevations in cytokines are associated with an increased risk of osteoarthritis [20,21].”
BackgroundCurrent Concepts and Future Directions of Minimally Invasive Treatment for Knee Pain
Goldman, D., Piechowiak, R., Nissman, D., Bagla, S., & Isaacson, A. (2018) · Current Rheumatology Reports · doi:10.1007/s11926-018-0765-x · Cited by 34
Ma, J., Guo, A., Wang, S., Man, S., Zhang, Y., Liu, S., & Liu, Y. (2018) · Journal of Hazardous Materials · doi:10.1016/j.jhazmat.2018.04.025 · Cited by 37
Rey-Rico, A., Venkatesan, J., Schmitt, G., Concheiro, A., Madry, H., Alvarez-Lorenzo, C., & Cucchiarini, M. (2017) · International Journal of Nanomedicine · doi:10.2147/ijn.s144579 · Cited by 34
“Introduction Osteoarthritis (OA) is a major, chronic joint disorder that involves deep changes in the structure and functions of skeletal tissues and cells, causing the gradual and irreversible breakdown of the articular cartilage (the end point of OA), the remodeling of the subchondral bone, and the formation of oste…”
Influence of osteoarthritis grade on molecular signature of human cartilage
Zhou, S., Thornhill, T., Meng, F., Xie, L., Wright, J., & Glowacki, J. (2016) · Journal of Orthopaedic Research · doi:10.1002/jor.23043 · Cited by 34
“There is a large body of knowledge derived from studies of human chondrocytes stimulated by pro-inflammatory Interleukins or TNF.7,16,36 In vitro treatment of normal articular chondrocytes with IL-1b, for example, induces them to express catabolic and matrix degradation factors.”
BackgroundInfluentialSunaga, T., Oh, N., Hosoya, K., Takagi, S., & Okumura, M. (2012) · Journal of Veterinary Medical Science · doi:10.1292/jvms.11-0511 · Cited by 34
“Interleukin-1β could stimulate overproduction of several catabolic molecules, including MMPs [2], then is thought to play an important role in manifestation of OA pathologies [4, 6, 10, 11, 17, 18].”
BackgroundFuruzawa-Carballeda, J., Lima, G., Llorente, L., Núñez-Álvarez, C., Ruiz-Ordaz, B., Echevarría-Zuno, S., & Hernández-Cuevas, V. (2012) · TheScientificWorldJournal · doi:10.1100/2012/342854 · Cited by 34
“(LIF), and chemokines have also been implicated [6].”
BackgroundNebbaki, S., Mansouri, F. E., Afif, H., Kapoor, M., Benderdour, M., Duval, N., Pelletier, J., Martel-Pelletier, J., & Fahmi, H. (2012) · Arthritis Research & Therapy · doi:10.1186/ar3788 · Cited by 34
“Indeed, Egr-1 mediates IL-1-induced mPGES-1 expression and PGE2 production in several cell types, including chondrocytes and synovial fibroblasts [22].”
BackgroundInfluentialSelf-citationRibeiro, R. A., Lima-Júnior, R., Leite, C. A., Mota, J. M., Macedo, F. D. B., Lima, M., & Brito, G. A. D. C. (2012) · doi:10.5455/jeim.080312.ir.010 · Cited by 34
“distress syndrome [73], osteoarthritis [74] and”
Xia, S., Li, L., Shi, Z., Sun, N., & He, Y. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1604652 · Cited by 33
Liang, C., Xing, H., Wang, C., Xu, X., Hao, Y., & Qiu, B. (2022) · Journal of Orthopaedic Surgery and Research · doi:10.1186/s13018-022-03306-y · Cited by 38
“The levels of various pro-inflammatory factors like IL-1β, IL-8, TNF-α, and IL-6 increase in OA joint tissues, with IL-1β being the most critical pro-inflammatory factor [16, 17].”
BackgroundMcKinney, J., Pucha, K., Doan, T., Wang, L., Weinstock, L. D., Tignor, B. T., Fowle, K. L., Levit, R., Wood, L., & Willett, N. (2021) · Acta Biomaterialia · doi:10.1016/j.actbio.2021.12.034 · Cited by 33
Thielen, N., Neefjes, M., Wiegertjes, R., van den Akker, G. V. D., Vitters, E., van Beuningen, H. V., Davidson, E. B., Koenders, M., van Lent, P., van de Loo, F. A., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22158124 · Cited by 33
Feng, Z.-Y., Hu, X.-J., Zheng, Q., Battié, M., Chen, Z., & Wang, Y. (2021) · Osteoarthritis and Cartilage · doi:10.1016/j.joca.2021.01.010 · Cited by 33
Blockade of IL‐33 signalling attenuates osteoarthritis
He, Z., Song, Y., Yi, Y.-X., Qiu, F., Wang, J., Li, J.-W., Jin, Q.-W., & Sacitharan, P. (2020) · Clinical & Translational Immunology · doi:10.1002/cti2.1187 · Cited by 33
“Increased joint inflammation caused by cytokines such as IL-1 and TNF-a has been shown to drive OA pathogenesis.(2,3) These cytokines increase the production of proteases by chondrocytes, the only resident cells in cartilage, to cause cartilage degradation and secondary disease symptoms such as pain.”
BackgroundWu, H., Zhang, M.-H., Li, W.-H., Zhu, S.-T., & Zhang, D.-F. (2020) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2020.109136 · Cited by 33
Haas, E. M., Eisele, A., Arnoldi, A., Paolini, M., Ehrl, D., Volkmer, E., & Giunta, R. (2020) · Plastic and Reconstructive Surgery · doi:10.1097/prs.0000000000006378 · Cited by 33
Dai, Z., Neogi, T., Brown, C. A., Nevitt, M. C., Lewis, C. E., Torner, J. C., & Felson, D. T. (2019) · The Journal of Rheumatology · doi:10.3899/jrheum.181365 · Cited by 40
“Accompanying this finding, shorter sleep duration was associated with higher levels of CRP (11, 35, 36), and CRP has been consistently associated with painful knee OA (5).”
BackgroundMa, D., Zhao, Y.-X., She, J., Zhu, Y.-D., Zhao, Y., Liu, L., & Zhang, Y.-G. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2019.03.001 · Cited by 33
Knockdown of FOXM1 attenuates inflammatory response in human osteoarthritis chondrocytes
Zeng, R.-M., Lu, X.-H., Lin, J., Hu, J., Rong, Z., Xu, W., Liu, Z., & Zeng, W. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2018.12.057 · Cited by 33
Lin, J., Li, X., Qi, W., Yan, Y.-Z., Chen, K., Xue, X., Xu, X.-X., Feng, Z.-H., & Pan, X. (2018) · International Immunopharmacology · doi:10.1016/j.intimp.2018.09.003 · Cited by 33
Ahmed, A., Gedin, P., Hugo, A., Bakalkin, G., Kanar, A., Hart, D., Druid, H., Svensson, C., & Kosek, E. (2018) · Journal of Immunology · doi:10.4049/jimmunol.1800486 · Cited by 33
“Synovial inflammation is a major source of proinflammatory cytokines, metalloproteinases (MMPs), and aggrecanases, which contribute to cartilage matrix degradation in OA (3, 4).”
BackgroundThe Protective Effect of Ligustilide in Osteoarthritis: An in Vitro and in Vivo Study
Li, X., Wu, D., Hu, Z., Xuan, J.-W., Ding, X.-X., Zheng, G., Feng, Z.-H., Ni, W., & Wu, A. (2018) · Cellular Physiology and Biochemistry · doi:10.1159/000492701 · Cited by 33
Vrgoč, G., Vrbanec, J., Eftedal, R., Dembic, P. L., Balen, S., Dembić, Z., & Jotanović, Z. (2018) · Journal of Orthopaedic Research · doi:10.1002/jor.23823 · Cited by 33
“Evidence suggests that IL-17 is involved in the early phase of the inflammatory process and induces the release of pro-inflammatory mediators in a several cell types.(5) It has been shown that IL-17 induces IL-1b, tumor necrosis factor-a (TNF-a), and IL-6 in chondrocytes which upregulate the production of nitric oxide…”
BackgroundInfluentialKwon, J., Lee, S.-H., Jhun, J., Choi, J., Jung, K., Cho, K.-H., Kim, S., Yang, C.-W., Park, S.-H., & Cho, M. (2018) · Journal of Medicinal Food · doi:10.1089/jmf.2017.4034 · Cited by 33
“Thus, the combination of probiotic complex, rosavin, and zinc has a potential to improve joint disability and pain induced by OA.”
InfluentialAborehab, N. M., Bishbishy, M. H. E., Refaiy, A. E., & Waly, N. E. (2017) · BMC Complementary and Alternative Medicine · doi:10.1186/s12906-017-2002-y · Cited by 33
Jia, P.-T., Zhang, X.-L., Zuo, H.-N., Lu, X., & Li, L. (2017) · Molecular Medicine Reports · doi:10.3892/mmr.2017.7340 · Cited by 33
“Inflammatory processes are associated with the degradation of cartilage and the subsequent development of OA (6).”
Liu, M.-R., Zhong, S.-Q., Kong, R., Shao, H., Wang, C., Piao, H.-Y., Lv, W., Chu, X., & Zhao, Y. (2017) · Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · doi:10.1016/j.biopha.2017.09.011 · Cited by 33
Jeong, H., Baek, S.-Y., Kim, S. W., Eun, Y., Kim, I., Lee, J., Jeon, C., Koh, E., & Cha, H. (2017) · PLoS ONE · doi:10.1371/journal.pone.0186141 · Cited by 33
Jeong, J.-W., Lee, H., Kim, J., Choi, E., Hwang-Bo, H., Kim, H., Kim, M. Y., Ahn, K., Kim, G.-Y., Lee, K.-W., et al. (2017) · Molecular Medicine Reports · doi:10.3892/mmr.2017.7075 · Cited by 33
“Compelling evidence has demonstrated that pro‑inflam-matory cytokines are significantly elevated in synovial fluid from patients with OA and have critical roles in the promotion of the catabolic processes in OA, causing cartilage degradation (31,40).”
Knockdown of TREM-1 suppresses IL-1β-induced chondrocyte injury via inhibiting the NF-κB pathway.
Tang, J., & Dong, Q.-R. (2017) · Biochemical and Biophysical Research Communications - BBRC · doi:10.1016/j.bbrc.2016.12.019 · Cited by 33
α2-Macroglobulin: Autologous Protease Inhibition Technology.
Cuéllar, J., Cuéllar, V. G., & Scuderi, G. (2016) · Physical Medicine and Rehabilitation Clinics of North America · doi:10.1016/j.pmr.2016.06.008 · Cited by 33
Discovery and evaluation of novel anti-inflammatory derivatives of natural bioactive curcumin
Zhang, Y.-L., Jiang, X., Peng, K., Chen, C., Fu, L.-L., Wang, Z., Feng, J.-P., Liu, Z.-G., Zhang, H., Liang, G., et al. (2014) · Drug Design, Development and Therapy · doi:10.2147/dddt.s69914 · Cited by 33
“Over-expressed inflammatory cytokines are involved in the pathological processes of a number of diseases.(1,2) In particular, sepsis, a systemic inflammatory response syndrome characterized by cytokine storm and multi-organ failure that occurs during severe infection, is believed to be related to an exacerbated releas…”
BackgroundAcquiring Chondrocyte Phenotype from Human Mesenchymal Stem Cells under Inflammatory Conditions
Kondo, M., Yamaoka, K., & Tanaka, Y. (2014) · International Journal of Molecular Sciences · doi:10.3390/ijms151121270 · Cited by 33
“etiologies of RA and OA are considered to be different, and both conditions develop distinct degrees and patterns of articular cartilage impairment; however, the pathophysiology of inflammation in the affected joints is similar in both diseases [23].”
BackgroundArticular Cartilage Changes in Maturing Athletes
Luria, A. R., & Chu, C. (2014) · Sports health · doi:10.1177/1941738113514369 · Cited by 33
“The lack of homeostasis in an aged joint leads to the progression of osteoarthritis.(67) Chondrocytes release chemoattractants such as IL-8 and monocyte chemoattractant protein 1 that direct the migration of leukocytes.”
BackgroundShin, K., Kim, J. W., Moon, K., Yang, J. A., Lee, E., Song, Y., & Lee, E. B. (2013) · Clinical Therapeutics · doi:10.1016/j.clinthera.2013.02.009 · Cited by 33
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Background
Metadata
- Authors
- Kapoor, M., Martel-Pelletier, J., Lajeunesse, D., Pelletier, J.-P., & Fahmi, H.
- Affiliations
- Hôpital Notre-Dame (CA)
- Venue
- Nature Reviews Rheumatology
- Published
- 2010-11-30
- Volume
- 7
- Issue
- 1
- Pages
- 33-42
- ISSN
- 1759-4790 (ISSN-L)
- 1759-4804
- OpenAlex
- W2038773696
- Cited by
- 2,778
- References
- 120
- Citations by year
- 2026: 207 · 2025: 232 · 2024: 252 · 2023: 271 · 2022: 249 · 2021: 252 · 2020: 234 · 2019: 199 · 2018: 175 · 2017: 141 · 2016: 145 · 2015: 128 · 2014: 106 · 2013: 83 · 2012: 73
- FWCI
- 7.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Rheumatology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
- Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Proteoglycans and glycosaminoglycans research
- Keywords
- osteoarthritis, inflammatory cytokines, IL-1β, TNF-α, interleukin-6, cartilage degeneration, subchondral bone remodeling, synovitis, anti-cytokine therapy, IL-17, IL-18, IL-21, leukemia inhibitory factor, interleukin-8
- MeSH terms
- Cartilage, Articular, Humans, Osteoarthritis, Tumor Necrosis Factor-alpha, Interleukin-6, Disease Progression, Interleukin-1beta
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