The Role of Sclerostin in Rheumatic Diseases: A Review

Jaśkiewicz, Łukasz; Chmielewski, Grzegorz; Kuna, Jakub; Stompór, Tomasz; Krajewska-Włodarczyk, Magdalena

doi:10.3390/jcm12196248

Cited by 3 publications

(2 citation statements)

References 123 publications

(150 reference statements)

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“…However, the literature reveals contradictory results regarding the relationship between sclerostin expression and bone loss in animal models of RA [ 4 , 5 , 7 ]. Likewise conflicting findings exist concerning sclerostin serum concentrations in RA patients [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Plasma Sclerostin Levels in Rheumatoid Arthritis Women on TNF-α Inhibitor Therapy

Szeremeta,

Jura-Półtorak,

Zoń-Giebel

et al. 2024

Pharmaceuticals

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Rheumatoid arthritis (RA) is associated with significant systemic and local bone loss. The aim of this study was to assess whether or not 15-month tumor necrosis factor α inhibitor (TNFαI) therapy in combination with methotrexate (MTX) affects circulating levels of sclerostin (SOST) in female RA patients. Plasma levels of SOST were measured using immunoassays kits. Baseline SOST levels showed no significant differences between RA patients and control participants. Postmenopausal women with RA tended to have higher sclerostin levels than premenopausal woman with RA. After 15 months of treatment with TNFαI, plasma levels of SOST were decreased. Before starting biological therapy, circulating levels of SOST significantly correlated with the patient’s age (p < 0.05) and the marker of inflammation, such as ESR (p < 0.05). Multivariate regression analysis showed that age was the only significant predictor for baseline SOST levels in women with RA (β = 0.008, p = 0.028, R2 model = 0.293). Moreover, a positive correlation between SOST levels and the 28 joint disease activity score value based on the erythrocyte sedimentation rate (DAS28-ESR) was found at baseline (p < 0.05), as well as after 15 months of biological therapy (p < 0.05). Thus, plasma SOST levels may be helpful for monitoring the efficacy of TNFαI treatment in RA patients. According to our results, TNFαI, in combination with MTX, has a beneficial effect on bone turnover with a significant reduction in bone metabolism marker SOST.

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Section: Introductionmentioning

confidence: 99%

Plasma Sclerostin Levels in Rheumatoid Arthritis Women on TNF-α Inhibitor Therapy

Szeremeta,

Jura-Półtorak,

Zoń-Giebel

et al. 2024

Pharmaceuticals

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“…These cells can secrete various cytokines, among which Th17 cells produce IL-17, which in turn activates other immune cells (such as fibroblasts and macrophages), promoting the release of IL-6, TNF-α, and other chemokines. 44 These inflammatory factors can further amplify the inflammation process of OA, ultimately exacerbating the condition. 45 This study conducted Mendelian randomization analysis using 731 immune cell subtypes as exposures, with OA and SAS as outcomes, finding that 57 immune cell phenotypes are associated with SAS, and 95 with OA.…”

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confidence: 99%

Association Between Sleep Apnea Syndrome and Osteoarthritis: Insights from Bidirectional Mendelian Randomization and Bioinformatics Analysis

Weng,

Luo,

Luo

et al. 2024

NSS

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Background: Sleep apnea syndrome(SAS) and osteoarthritis (OA) are two prevalent diseases that often coexist, but the causal relationship between them remains unclear. In light of this, our team utilizes Mendelian Randomization and bioinformatics analysis methods to investigate the potential association between the two diseases. Methods: In this study, we utilized GWAS data pertaining to SAS and OA to assess the causal relationship between the two diseases through Mendelian randomization (MR) analysis. We then employed transcriptomic data to perform differential gene identification, WGCNA, shared gene determination, functional enrichment analysis, and colocalization analysis, all designed to further elucidate the mechanisms underlying the association between the two diseases. In the end, we utilized Mendelian randomization (MR) analysis again to delve deeper into the relationship between the two diseases and immune cells. Results: Our research findings indicate that SAS is a risk factor for OA (p = 0.000004), knee OA (p = 0.0000001) and hip OA (p = 0.001). Furthermore, OA (p = 0.000195), knee OA (p = 0.001) are significant risk factors for SAS. However, there is no clear evidence that hip OA (p = 0.892) is a risk factor for SAS. Interestingly, the genes shared between OA and SAS are significantly enriched in leukocyte migration, leukocyte chemotaxis. Moreover, colocalization analysis suggests that the genes JUNB, COL8A1, FOSB, and IER2 may be key genes associated with both diseases. Furthermore, 57 immune cell phenotypes are associated with SAS, 95 with OA, and 6 shared between both diseases. Conclusion: This research confirmed the bidirectional causal relationship between SAS and OA. Notably, the 4 genes (JUNB, COL8A1, FOSB, IER2) and 6 immune phenotypes are crucial for both diseases, these provide hopeful targets for future interventions against these two diseases.

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Klotho protein, fibroblast growth factor 23, and sclerostin in chronic heart failure: literature review

Alieva,

Reznik,

Kotikova

et al. 2024

CardioSomatics

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Chronic heart failure (CHF) is a global medical, social, and economic problem. It is a syndrome caused by imbalanced neurohumoral regulation of the cardiovascular system, which is accompanied by impaired systolic and/or diastolic function of the heart. Currently, the search and study of new biological markers that can help in the early diagnosis of CHF, serve as a laboratory tool for assessing treatment effectiveness, or be used as prognostic markers and risk stratification criteria are ongoing. Researchers focused on studying the role of Klotho protein, fibroblast growth factor 23 (FGF23), and sclerostin in patients with CHF. Klotho expression decreases as the body ages, and impaired production has been reported in various aging-related diseases. The FGF23 / Klotho axis plays a key regulatory role in cardiovascular pathology. Laboratory, clinical, and genetic studies have suggested that sclerostin is associated with heart disease, although available data are not entirely consistent. Clinical work conducted on the study of the Klotho protein, FGF-23, and sclerostin indicates the potentially important diagnostic and prognostic significance of their analysis in patients with CHF. Thus, more studies of the issues related to serial testing of these biological markers, including in the aspect of the multibiomarker model, are needed.

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The Role of Sclerostin in Rheumatic Diseases: A Review

Cited by 3 publications

References 123 publications

Plasma Sclerostin Levels in Rheumatoid Arthritis Women on TNF-α Inhibitor Therapy

Plasma Sclerostin Levels in Rheumatoid Arthritis Women on TNF-α Inhibitor Therapy

Association Between Sleep Apnea Syndrome and Osteoarthritis: Insights from Bidirectional Mendelian Randomization and Bioinformatics Analysis

Klotho protein, fibroblast growth factor 23, and sclerostin in chronic heart failure: literature review

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