2022
DOI: 10.1016/j.bonr.2022.101599
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Serum biomarkers for arterial calcification in humans: A systematic review

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Cited by 12 publications
(6 citation statements)
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References 143 publications
(395 reference statements)
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“…Several clinical studies have investigated the possible association between OPG and arterial calci cation. Out of these studies, 19 reported a positive association, 2 reported negative association and 17 reported no association at all [15].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Several clinical studies have investigated the possible association between OPG and arterial calci cation. Out of these studies, 19 reported a positive association, 2 reported negative association and 17 reported no association at all [15].…”
Section: Discussionmentioning
confidence: 99%
“…Mediators of bone metabolism seem to play an active role in this transformation process. This medial calci cation leads to arterial stiffening which in turn results in cardiovascular disease [15]. OPG and RANKL, which are important regulators of bone metabolism are also considered to be involved in ectopic mineralization.…”
Section: Discussionmentioning
confidence: 99%
“…Most studies are of a poor quality, were mainly cross-sectional, and were influenced by confounding factors. The most recent meta-analysis included several biomarkers: calcium, phosphate, parathyroid hormone, vitamin D, pyrophosphate, OPG, RANKL, FGF-23, Klotho, osteopontin, osteocalcin, MGP and its inactive forms, and vitamin K. Of all the markers included, phosphate, osteopontin, and FGF-23 were found to be suitable biomarkers for MAC [ 124 ]. However, further studies are needed to test their predictive value for the development of MAC.…”
Section: Conclusion and Future Perspectivesmentioning
confidence: 99%
“…Цікаво, що блокування остеохондрогенного диференціювання VSMC впливало на кальцифікацію, але не на системний ліпідний обмін, експресію ліганда активатора рецептора ядерного фактора каппа-В (RANKL), залучення моноцитів/макрофагів або розмір атеросклеротичного ураження. Ці дані вперше виявили генетичний поділ між кальцифікуючим склеротичним процесом і ліпідним, атерогенним процесом, надаючи змогу припустити, що різні механізми регулюють формування та прогресування кальцифікації та атероми відповідно до відмінностей в етіології між ІАК та атерогенезом [51].…”
Section: вплив окиснювального стресу та мітохондріальної дисфункції н...unclassified