PCSK9 IN ATHEROSCLEROSIS (DSB.AD006.171)

Area tematica

Scienze biomediche

Area progettuale

Struttura responsabile del progetto di ricerca

Istituto di fisiologia clinica (IFC)

Responsabile di progetto

CHIARA CASELLI
Telefono: 0503153551
E-mail: caselli@ifc.cnr.it

Abstract

Reduction in low-density lipoprotein cholesterol (LDL-C), has decreased the risk of cardiovascular events over the last few decades. However, many individuals treated with statins do not achieve their target levels of LDL-C, and thus, LDL-associated residual risk remains. Gain of function mutations of the proprotein convertase subtilisin/kexin type 9 (PCSK9) by enhancing degradation of the hepatic LDL receptor (LDLR), are associated with high plasma LDL-C levels and increased risk of cardiovascular events. Inhibition of PCSK9 alone or in addition to statins potently reduces serum LDL-C concentrations, by 50-70%. Experimental studies have shown a key role of PCSK9 in atherosclerosis by mechanisms independent of LDLR. We hypothesize that effects of PCSK9 modulation may extend beyond LDL-C reduction. The purpose of the present proposal is to evaluate the consequences of interferences with PCSK9 on processes implicated in atherosclerosis at molecular level. This project will extend knowledge and understanding of the effects of PCSK9 interference on the pathogenetic mechanisms of atherosclerosis.

Obiettivi

The purpose of the present proposal is to evaluate the consequences of interferences with PCSK9 on processes implicated in atherosclerosis, such as endothelial dysfunction and inflammation, at the molecular level. The possible additional effects of PCSK9 inhibition beyond the actions of statins will also be evaluated.

Data inizio attività

01/06/2017

Parole chiave

PCSK9, atherosclerosis

Ultimo aggiornamento: 19/04/2024