Abstract
BackgroundSclerostin 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.MethodsFasting 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.ResultsThirty-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 R2 change: 0.146, p = 0.003) was positively associated with cfPWV values in patients with hypertension.ConclusionsIn 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.
Highlights
Sclerostin is known to be a canonical Wnt/β-catenin signaling pathway inhibitor, while the Wnt/βcatenin signaling pathway is proposed to be involved in the development of arterial stiffness
Systolic blood pressures (BP) (SBP) and diastolic BP (DBP) values were recorded at the points of appearance and disappearance of the Korotkoff sounds, respectively
Our forward multivariable logistic regression analysis, after adjusting for the factors significantly associated with arterial stiffness showed that sclerostin, age, and iPTH were independent predictors of arterial stiffness in hypertensive patients (Table 2)
Summary
Sclerostin is known to be a canonical Wnt/β-catenin signaling pathway inhibitor, while the Wnt/βcatenin signaling pathway is proposed to be involved in the development of arterial stiffness. Several studies have reported arterial stiffness to be closely related to cardiovascular morbidity and mortality in hypertensive patients [2,3,4]. These evidences seem to point towards the Arterial stiffness, which results from progressive breakdown of elastic fibers in the aorta and large elastic arteries, causes increased pulse wave velocity (PWV), decreased diastolic coronary perfusion pressure, and will eventually lead to diminished myocardial oxygen delivery [6, 7]. Carotid–femoral PWV (cfPWV), calculated as the time required for arterial pulse to spread from the carotid to the femoral artery, can be used to measure central arterial stiffness [8]. CfPWV has been recommended as a tool for the diagnosis of target organ damage in patients with earlier stages of hypertension [10]
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