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dc.contributor.authorAlsheikh-Ali, Alawi A.
dc.date.accessioned2021-03-10T11:46:27Z
dc.date.available2021-03-10T11:46:27Z
dc.date.issued2017-03-30
dc.identifier.other204-2017.28
dc.identifier.urihttps://repository.mbru.ac.ae/handle/1/200
dc.description.abstractAbstract: Lipoprotein(a), or Lp(a), significantly increased alkaline phosphatase activity, release of phosphate, calcium deposition, hydroxyapatite, cell apoptosis, matrix vesicle formation, and phosphorylation of signal transduction proteins; increased expression of chondro-osteogenic mediators; and decreased SOX9 and matrix Gla protein (p < 0.001). Inhibition of MAPK38 and GSK3b significantly reduced Lp(a)-induced calcification of human aortic valve interstitial cells (p < 0.001). There was abundant presence of Lp(a) and E06 immunoreactivity in diseased human aortic valves. The present study demonstrates a causal effect for Lp(a) in aortic valve calcification and suggests that interfering with the Lp(a)pathway could provide a novel therapeutic approach in the management of this debilitating disease.en_US
dc.language.isoenen_US
dc.subjectLipoproteinen_US
dc.subjectAortic Valveen_US
dc.subjectInterstitial Cell Calcificationen_US
dc.titleLipoprotein(a) Induces Human Aortic Valve Interstitial Cell Calcificationen_US
dc.typeArticleen_US


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