Key result
High expression of the Pi-transporter SLC20A1 in calcific aortic valve disease promotes apoptosis and mineralization by down-regulating Akt-1.
Why the study?
Does high expression of SLC20A1 promote mineralization and apoptosis in valve interstitial cells through regulation of Akt-1?
Observational (n=78)
Does high expression of SLC20A1 promote mineralization and apoptosis in valve interstitial cells through regulation of Akt-1?
The phosphate transporter SLC20A1 is highly expressed in calcific aortic valve disease and promotes valve interstitial cell mineralization and apoptosis by downregulating Akt-1.
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Hypothesis-generating for SLC20A1 inhibition in aortic valve calcification; should not change practice pending clinical validation.
Husseini et al. (2013) conducted an observational in Calcific Aortic Valve Disease (n=78). High expression of SLC20A1/Pit1 vs. Control non-mineralized aortic valves was evaluated on Expression of SLC20A1 and Akt-1 in CAVD tissues and in vitro mineralization. High expression of the Pi-transporter SLC20A1 in calcific aortic valve disease promotes apoptosis and mineralization by down-regulating Akt-1.
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