Abstract
Lipoprotein(a), or Lp(a), significantly increased alkaline phosphatase activity, release of phosphate, calcium deposition, hydroxyapatite, cell apoptosis, matrix vesicle formation, and phosphorylation of signaltransduction proteins; increased expression of chondro-osteogenic mediators; and decreased SOX9and matrix Gla protein (p<0.001). Inhibition of MAPK38 and GSK3β 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 forLp(a) in aortic valve calcification and suggests that interfering with the Lp(a)pathway couldprovide anovel therapeutic approach in the management of this debilitating disease.
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