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The association between Hepcidin and arterial stiffness in a community-dwelling population

BACKGROUND: An association of hepcidin with cardiovascular (CV) disease and atherosclerosis has been reported in different patient groups. However, it has not been well described clinically the association between hepcidin and arterial stiffness. In this study,We analysed the possible mechanism of H...

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Detalles Bibliográficos
Autores principales: Wang, Xiaona, Sheng, Li, Ye, Ping, Cao, Ruihua, Yang, Xu, Xiao, Wenkai, Zhang, Yun, Bai, Yongyi, Wu, Hongmei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6206657/
https://www.ncbi.nlm.nih.gov/pubmed/30373612
http://dx.doi.org/10.1186/s12944-018-0866-6
Descripción
Sumario:BACKGROUND: An association of hepcidin with cardiovascular (CV) disease and atherosclerosis has been reported in different patient groups. However, it has not been well described clinically the association between hepcidin and arterial stiffness. In this study,We analysed the possible mechanism of Hepcidin and arterial stiffness. METHODS: This article related measurements of plasma hepcidin and arterial stiffness (carotid–femoral pulse wave velocity [PWV]) in a community-based sample. RESULTS: After a median follow-up interval of 4.8 years, multiple linear regression analysis revealed that hepcidin was independently associated with carotid–femoral PWV (β = 1.498, P < 0.001). In a multivariable linear regression analysis, HDL3-C levels were negatively and independently associated with hepcidin at baseline (β = − 0.857, P = 0.024). HDL2-C was not associated with hepcidin at baseline (β = − 1.121, P = 0.133). CONCLUSIONS: We found an association between baseline hepcidin and follow-up arterial stiffness that was independent of age, gender and other vascular risk factors. We also identified an association between hepcidin and HDL3-C at baseline, which indicates that the HDL3-C level may reflect the change in cholesterol efflux from peripheral arteries and partly explain the relationship between hepcidin and the change of arterial stiffness.