Clinical Significance of Resistin Expression in Osteoarthritis: A Meta-Analysis

Li, Xiaochuan; Tian, Feng; Wang, Fei

doi:10.1155/2014/208016

Cited by 17 publications

(15 citation statements)

References 39 publications

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“…Much of the previous research in osteoarthritis suggested higher circulating adipokine levels in osteoarthritis patients [ 39 – 44 ], and although we observed higher adiponectin and leptin levels in participants with osteoarthritis, only adiponectin resulted in a significant association with osteoarthritis. It is worth noting that the extent of osteoarthritis may influence adipokine levels as associations with adipokines and grading or severity of disease have been documented [ 12 , 40 , 42 ].…”

Section: Discussioncontrasting

confidence: 66%

Adiposity Measures and Plasma Adipokines in Females with Rheumatoid and Osteoarthritis

DeClercq

Cui

Forbes

et al. 2017

Mediators of Inflammation

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The objective of this study was to examine the relationship between adipokines and adiposity in individuals with rheumatoid and osteoarthritis in the Atlantic PATH cohort. Using a nested case-control analysis, participants in the Atlantic PATH cohort with rheumatoid or osteoarthritis were matched for measures of adiposity with participants without a history of arthritis. Both measured and self-reported data were used to examine disease status, adiposity, and lifestyle factors. Immunoassays were used to measure plasma markers. BMI was positively correlated with percentage body fat, fat mass index (FMI), and a change in BMI from 18 years of age in all 3 groups. There were no statistical differences between levels of plasma adipokines; adiponectin levels were 6.6, 7.9, and 8.2 μg/ml, leptin levels were 10.3, 13.7, and 11.5 ng/ml, and resistin levels were 10.0, 12.1, and 10.8 ng/ml in participants without arthritis, with rheumatoid arthritis, and with osteoarthritis, respectively. Those with higher levels of adiponectin were more likely to have osteoarthritis (but not rheumatoid arthritis). No association was found between arthritis types and leptin or resistin. This study demonstrates differences in measures of adiposity and adipokines in specific types of arthritis and highlights the need for more research targeting specific adipokines during arthritic disease progression.

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Section: Discussioncontrasting

confidence: 66%

Adiposity Measures and Plasma Adipokines in Females with Rheumatoid and Osteoarthritis

DeClercq

Cui

Forbes

et al. 2017

Mediators of Inflammation

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“…In the obesity-induced model of osteoarthritis in mice the pro-inflammatory cytokines adiponectin, resistin and IL-6 [49][50][51][52] contribute to the chondrocyte and cartilage defects observed and these and other adipokines have been proposed as biomarkers of osteoarthritis. Despite the contribution of these cytokines to the pathogenesis of OA, A2AR stimulation reverses the osteoarthritis that develops in obese mice without affecting serum levels of these adipokines.…”

Section: Discussionmentioning

confidence: 99%

Intraarticular injection of liposomal adenosine reduces cartilage damage in established murine and rat models of osteoarthritis

Corciulo

Castro

Coughlin

et al. 2020

Sci Rep

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Osteoarthritis (OA) affects nearly 10% of the population of the United States and other industrialized countries and, at present, short of surgical joint replacement, there is no therapy available that can reverse the progression of the disease. Adenosine, acting at its A2A receptor (A2AR), is a critical autocrine factor for maintenance of cartilage homeostasis and here we report that injection of liposomal suspensions of either adenosine or a selective A2AR agonist, CGS21680, significantly reduced oA cartilage damage in a murine model of obesity-induced oA. the same treatment also improved swelling and preserved cartilage in the affected knees in a rat model of established posttraumatic OA (PTOA). Differential expression analysis of mRNA from chondrocytes harvested from knees of rats with PTOA treated with liposomal A2AR agonist revealed downregulation of genes associated with matrix degradation and upregulation of genes associated with cell proliferation as compared to liposomes alone. Studies in vitro and in affected joints demonstrated that A2AR ligation increased the nuclear P-SMAD2/3/P-SMAD1/5/8 ratio, a change associated with repression of terminal chondrocyte differentiation. These results strongly suggest that targeting the A2AR is an effective approach to treat oA. Osteoarthritis (OA) is a common disease affecting 151 million people worldwide and its incidence is expected to increase in industrialized countries due to aging and increased obesity of the population, a condition that together with previous joint injury represent the most common risk factors 1. OA can affect any joint, but most commonly affects the knee, hip and hand. The prevalence of OA is greatest in the knee joint, in both women (47%) and men (40%), and there is no therapy currently available that can reverse or halt the progression of OA 2,3 short of total joint replacement. Total knee replacements are the most common joint surgeries and it has been estimated that there will be a fivefold increase in the number of patients undergoing this surgical procedure up to 3.5 million by 2030 4,5. In search of effective therapies, a number of different approaches have been taken including a focus on both growth factors, such as transforming growth factor-beta (TGFβ), and other molecular pathways involved in regulating cartilage development and homeostasis. TGFβ molecular signaling exerts dual and opposing roles in cartilage and chondrocyte health depending on the receptor and signal activated downstream. It has been shown that inhibition of high levels of systemic TGFβ attenuates anterior cruciate ligament rupture-induced OA in mice by preventing loss of proteoglycan from the cartilage and protecting the subchondral bone from structural alteration 6. Moreover, the effect of TGFβ on joint health depends on which receptor it binds. Activation of

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“…The current studies mostly support the notion that human resistin is highly secreted and exerts proinflammatory actions in OA. Thus far, there is only a recent meta-analysis published in 2014, which reported that high resistin expression represents a significant and reproducible marker of rapid disease progression in OA patients, especially male patients [37]. They just summarize resistin expression linked with OA; however, the role of resistin in the pathogenesis of OA has not yet been systematically elucidated.…”

Section: Introductionmentioning

confidence: 99%

An Update on the Emerging Role of Resistin on the Pathogenesis of Osteoarthritis

Zhao

Gao

Song

et al. 2019

Mediators of Inflammation

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Background. Resistin may be involved in the pathogenesis of osteoarthritis (OA), but a systematic understanding of the role of resistin in OA is lacking. Methods. We reviewed studies that evaluated the role of resistin in OA. The expression levels of resistin in vitro experiments and OA/rheumatoid arthritis (RA) patients were analyzed. We also studied potential resistin receptors and the signaling pathways that these receptors activate, ultimately leading to cartilage degeneration. Results. Resistin levels in both the serum and synovial fluid were higher in OA and RA patients than in healthy subjects. Overall, resistin levels are much higher in serum than in synovial fluid. In human cartilage, resistin induces the expression of proinflammatory factors such as degradative enzymes, leading to the inhibition of cartilage matrix synthesis, perhaps by binding to Toll-like receptor 4 and the adenylyl cyclase-associated protein 1 receptor, which then activates the p38-mitogen-activated phosphate kinase, protein kinase A–cyclic AMP, nuclear factor-κB, and C/enhancer-binding protein β signaling pathways. Conclusion. Resistin levels are higher in OA patients than in healthy controls; however, the precise role of resistin in the pathogenesis of OA needs to be studied further. Resistin may be a novel therapeutic target in OA in the future.

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Clinical Significance of Resistin Expression in Osteoarthritis: A Meta-Analysis

Cited by 17 publications

References 39 publications

Adiposity Measures and Plasma Adipokines in Females with Rheumatoid and Osteoarthritis

Adiposity Measures and Plasma Adipokines in Females with Rheumatoid and Osteoarthritis

Intraarticular injection of liposomal adenosine reduces cartilage damage in established murine and rat models of osteoarthritis

An Update on the Emerging Role of Resistin on the Pathogenesis of Osteoarthritis

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