Current advances in therapies for osteoarthritis

Kalunian, Kenneth C.

doi:10.1097/bor.0000000000000273

Cited by 27 publications

(25 citation statements)

References 19 publications

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“…Its prevalence has doubled since the mid‐20th century, yet it is still poorly understood (Ondrésik et al, ; Wallace et al, ). OA is a degenerative joint disease characterized by articular cartilage degradation (Kalunian, ), which causes pain, stiffness, and even disability of joints (Garstang & Stitik, ; Wang et al, ).…”

Section: Introductionmentioning

confidence: 99%

Mechanical stress protects against osteoarthritis via regulation of the AMPK/NF‐κB signaling pathway

Yang

Wang

Kong

et al. 2018

Journal Cellular Physiology

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Mechanical stress plays a key role in regulating cartilage degradation in osteoarthritis (OA). The aim of this study was to evaluate the effects and mechanisms of mechanical stress on articular cartilage. A total of 80 male Sprague‐Dawley rats were randomly divided into eight groups ( n = 10 for each group): control group (CG), OA group (OAG), and CG or OAG subjected to low‐, moderate‐, or high‐intensity treadmill exercise (CL, CM, CH, OAL, OAM, and OAH, respectively). Chondrocytes were obtained from the knee joints of rats; they were cultured on Bioflex 6‐well culture plates and subjected to different durations of cyclic tensile strain (CTS) with or without exposure to interleukin‐1β (IL‐1β). The results of the histological score, immunohistochemistry, enzyme‐linked immunosorbent assay, and western‐blot analyses indicated that there were no differences between CM and CG, but OAM showed therapeutic effects compared with OAG. However, CH and OAH experienced more cartilage damage than CG and OAG, respectively. CTS had no therapeutic effects on collagen II of normal chondrocytes, which is consistent with findings after treadmill exercise. However, CTS for 4 hr could alleviate the chondrocyte damage induced by IL‐1β by activating AMP‐activated protein kinase (AMPK) phosphorylation and suppressing nuclear translocation of nuclear factor (NF)‐κB p65. Our findings indicate that mechanical stress had no therapeutic effects on normal articular cartilage and chondrocytes; mechanical stress only caused damage with excessive stimulation. Still, moderate biomechanical stress could reduce sensitization to the inflammatory response of articular cartilage and chondrocytes through the AMPK/NF‐κB signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Mechanical stress protects against osteoarthritis via regulation of the AMPK/NF‐κB signaling pathway

Yang

Wang

Kong

et al. 2018

Journal Cellular Physiology

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“…МТ представляет большой интерес и для лечения ОА, с учетом роли хронического воспаления в развитии боли и прогрессирования структурных изменений при этом заболевании [52]. Имеется небольшой, но крайне интересный опыт применения МТ при ОА.…”

Section: глюкокортикоидыunclassified

Pain and Inflammation. Part 2. The Analgesic Potential of Anti-Inflammatory Drugs

Каратеев¹,

Каратеев²,

Davydov³

2017

rsp

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“…1 Articular cartilage degeneration, subchondral sclerosis and synovial inflammation are the characteristics of osteoarthritis. 2 The etiology of osteoarthritis is multifactorial, including aging, strain, trauma, infection, obesity, joint congenital anomalies, metabolic disease, and so on. 3,4 Osteoarthritis increases with the prolongation of lifespan and has become one of the global clinical problems that burden patients and health care systems.…”

Section: Introductionmentioning

confidence: 99%

<p>Downregulation of miR-34a Promotes Proliferation and Inhibits Apoptosis of Rat Osteoarthritic Cartilage Cells by Activating PI3K/Akt Pathway</p>

Tao¹,

Cheng²,

Yang³

2020

CIA

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Objective: To elucidate the expression and function of miR-34a in rat osteoarthritic cartilage cells, and further to explore its mechanism. Material and Methods: Rat model of osteoarthritis was constructed and knee joint cartilage cells were isolated in vitro. Immunocytochemical staining was used for identification. qRT-PCR was used to detect the expression of miR-34a in cartilaginous tissues and cartilage cells. Cartilage cells were divided into blank control (BC), negative control (NC), miR-34a inhibitor (34aI), osteoarthritis model (OA), osteoarthritis model + negative control (OA + NC) and osteoarthritis model + miR-34a inhibitor (OA + 34aI) groups. Cell proliferation was detected by CCK-8 and colony formation assays. Cell apoptosis was studied by flow cytometry and Western blot. PI3K/AKT-pathway-related proteins were also analyzed by Western blot. To further validate the effect of miR-34a on the PI3K/Akt pathway, the cartilage cells were divided into blank control (BC), osteoarthritis model (OA), osteoarthritis model + miR-34a inhibitor (OA + 34aI), osteoarthritis model + PI3K activator (OA + IGF-1) and osteoarthritis model + miR-34a inhibitor + PI3K inhibitor (OA + 34aI + LY) groups, the experiments above were repeated. Results: The expression of miR-34a in cartilaginous tissues and cells of osteoarthritis model was significantly higher than that in normal (p < 0.05). After silencing miR-34a gene, the cell proliferation and proteins expression of PI3K/Akt pathway were increased, while the apoptosis rate and expression of apoptosis-related proteins were decreased. Addition of PI3K activator also evidently promoted proliferation and inhibited apoptosis. The protein expression of Bax, Cleaved caspase-3 and Cleaved caspase-9 were dramatically decreased, while the ratios of p-PI3K/PI3K and p-Akt/Akt were increased in OA + IGF-1 group. Conclusion: Downregulation of miR-34a regulated proliferation and apoptosis of cartilage cells by activating PI3K/Akt pathway, providing a potential therapeutic approach for the treatment of osteoarthritis.

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Current advances in therapies for osteoarthritis

Abstract: Advances in the understanding of key areas of osteoarthritis pathogenesis are helping define the spectrum of therapeutic targets that potentially should be explored to reduce the symptomatic and structural effects of osteoarthritis.

Cited by 27 publications

References 19 publications

Mechanical stress protects against osteoarthritis via regulation of the AMPK/NF‐κB signaling pathway

Mechanical stress protects against osteoarthritis via regulation of the AMPK/NF‐κB signaling pathway

Pain and Inflammation. Part 2. The Analgesic Potential of Anti-Inflammatory Drugs

<p>Downregulation of miR-34a Promotes Proliferation and Inhibits Apoptosis of Rat Osteoarthritic Cartilage Cells by Activating PI3K/Akt Pathway</p>

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