Abstract
The studies in this thesis support the notion that Lipoprotein(a) [Lp(a)] metabolism is driven primarily by production and that catabolism plays a smaller role. The catabolic rates for the apo(a) and apoB proteins within Lp(a) particles seem to be tightly coupled. In addition, the catabolic rate is slower for Lp(a) than for LDL-apoB following apheresis, which suggests that the LDL-receptor does not play a major role in Lp(a) catabolism.These findings should be extended by investigating the kinetic associations between Lp(a) and other atherogenic lipoproteins and the mechanisms of actions of newer therapies especially apo(a) RNA based therapies.
Original language | English |
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Qualification | Doctor of Philosophy |
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Award date | 24 Aug 2020 |
DOIs | |
Publication status | Unpublished - 2020 |