Lipoprotein(a) significantly increased alkaline phosphatase activity, calcium deposition, and apoptosis in human aortic valve interstitial cells, demonstrating a causal effect in aortic valve calcification.
p-value: p=<0.001
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 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 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.
Yu et al. (Tue,) conducted a other in Aortic valve calcification (n=112). Lipoprotein(a) vs. Control medium was evaluated on Alkaline phosphatase activity, calcium deposition, and osteogenic differentiation (p=<0.001). Lipoprotein(a) significantly increased alkaline phosphatase activity, calcium deposition, and apoptosis in human aortic valve interstitial cells, demonstrating a causal effect in aortic valve calcification.