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Serum levels of sclerostin as a potential biomarker in central arterial stiffness among hypertensive patients. | LitMetric

Background: Sclerostin is known to be a canonical Wnt/β-catenin signaling pathway inhibitor, while the Wnt/β-catenin signaling pathway is proposed to be involved in the development of arterial stiffness. This study aims to investigate the relationship between serum sclerostin levels and carotid-femoral pulse wave velocity (cfPWV) among hypertensive patients.

Methods: Fasting blood samples were obtained from 105 hypertensive patients. Patients with cfPWV values of > 10 m/s were classified in the high arterial stiffness group, whereas those with cfPWV values of ≤10 m/s were assigned to the low arterial stiffness group. Serum sclerostin and Dickkopf-1 (DKK1) levels were quantified using commercially available enzyme-linked immunosorbent assays.

Results: Thirty-six hypertensive patients (34.3%) who belonged to the high arterial stiffness group were generally older (p < 0.001), presented with lower estimated glomerular filtration rates (eGFR, p = 0.014), higher incidence of diabetes mellitus (p = 0.030), average systolic blood pressures (SBP, p = 0.013), pulse pressure (p = 0.026), serum creatinine levels (p = 0.013), intact parathyroid hormone levels (iPTH, p = 0.003), and sclerostin levels (p < 0.001) than their counterparts in the low arterial stiffness group. A multivariable logistic regression analysis identified sclerostin as an independent predictor of arterial stiffness in hypertensive patients (odds ratio, 1.042; 95% confidence interval (CI), 1.017-1.068; p = 0.001). Multivariable forward stepwise linear regression analysis also showed that serum sclerostin level (β = 0.255, adjusted R change: 0.146, p = 0.003) was positively associated with cfPWV values in patients with hypertension.

Conclusions: In this study, serum sclerostin level, but not DKK1, is found to be positively correlated with cfPWV values and is identified as an independent predictor of arterial stiffness in hypertensive patients after adjusting for significant confounders.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6260557PMC
http://dx.doi.org/10.1186/s12872-018-0955-5DOI Listing

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