دورية أكاديمية

Pathophysiology of vascular calcification and bone loss: linked disorders of ageing?

التفاصيل البيبلوغرافية
العنوان: Pathophysiology of vascular calcification and bone loss: linked disorders of ageing?
المؤلفون: Cannata-Andía, Jorge B., Carrillo-López, Natalia, Messina, Osvaldo D., Hamdy, Neveen A. T., Panizo, Sara, Ferrari, Serge Livio
المصدر: ISSN: 2072-6643 ; Nutrients, vol. 13, no. 11 (2021) 3835.
سنة النشر: 2021
المجموعة: Université de Genève: Archive ouverte UNIGE
مصطلحات موضوعية: info:eu-repo/classification/ddc/616, Bone fractures, Bone loss, Fracture risk, Mineral bone disorders, Osteoporosis, Vascular calcification
الوصف: Vascular Calcification (VC), low bone mass and fragility fractures are frequently observed in ageing subjects. Although this clinical observation could be the mere coincidence of frequent age-dependent disorders, clinical and experimental data suggest that VC and bone loss could share pathophysiological mechanisms. Indeed, VC is an active process of calcium and phosphate precipitation that involves the transition of the vascular smooth muscle cells (VSMCs) into osteoblast-like cells. Among the molecules involved in this process, parathyroid hormone (PTH) plays a key role acting through several mechanisms which includes the regulation of the RANK/RANKL/OPG system and the Wnt/ß-catenin pathway, the main pathways for bone resorption and bone formation, respectively. Furthermore, some microRNAs have been implicated as common regulators of bone metabolism, VC, left ventricle hypertrophy and myocardial fibrosis. Elucidating the common mechanisms between ageing; VC and bone loss could help to better understand the potential effects of osteoporosis drugs on the CV system.
نوع الوثيقة: article in journal/newspaper
اللغة: English
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/34836090; https://archive-ouverte.unige.ch/unige:161398Test; unige:161398
الإتاحة: https://doi.org/10.3390/nu13113835Test
https://archive-ouverte.unige.ch/unige:161398Test
حقوق: info:eu-repo/semantics/openAccess
رقم الانضمام: edsbas.20833A7E
قاعدة البيانات: BASE