Abstract
Background and Aims: PCSK9 is a plasma glycoprotein mainly produced by the liver which, interacting with lipids and lipoprotein receptors such as LDLR receptor(s) and CD36, can regulate their degradation. PCSK9 deficiency induces an increase in the uptake of lipoproteins, promoting the removal of circulating lipids and their accumulation in different tissues. Given the impact of PCSK9 inhibitors as a modulator of plasma lipoprotein, levels the present work was aimed to evaluate its role on cardiac functionality and metabolism.
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