Key result
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.
Why the study?
Does Lipoprotein(a) induce calcification in human aortic valve interstitial cells?
Does Lipoprotein(a) induce calcification in human aortic valve interstitial cells?
p-value: p=<0.001
Lipoprotein(a) directly induces calcification in human aortic valve interstitial cells, providing mechanistic evidence for its causal role in calcific aortic valve disease and highlighting a potential therapeutic target.
Supports Lp(a) targeting in aortic stenosis; hypothesis-generating from in vitro data, requiring in vivo confirmation.
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.
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Yu et al. (2017) studied 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.
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