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2017 ; 12
(Suppl 1
): 2-11
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PCSK9 targets important for lipid metabolism
#MMPMID28176216
Schulz R
; Schlüter KD
Clin Res Cardiol Suppl
2017[Mar]; 12
(Suppl 1
): 2-11
PMID28176216
show ga
Ischemic heart disease is the main cause of death worldwide and it is accelerated
by increased low-density lipoprotein (LDL) cholesterol (LDL-C) and/or lipoprotein
(a) (Lp(a)) concentrations. Proprotein convertase subtilisin/kexin type 9 (PCSK9)
alters both LDL-C and in part Lp(a) concentrations through its ability to induce
degradation of the LDL receptor (LDLR). PCSK9, however, has additional targets
which are potentially involved in lipid metabolism regulation such as the very
low density lipoprotein receptor (VLDL), CD36 (cluster of differentiation 36) and
the epithelial cholesterol transporter (NPC1L1) and it affects expression of
apolipoprotein B48. The PCSK9 activity is tightly regulated at several levels by
factors influencing its transcription, secretion, or by extracellular
inactivation and clearance. Many comorbidities (kidney insufficiency,
hypothyreoidism, hyperinsulinemia, inflammation) modify PCSK9 expression and
release. Two humanized antibodies directed against extracellular PCSK9 received
approval by the European and US authorities and additional PCSK9 directed
therapeutics (such as silencing RNA) are already in clinical trials. Their
results demonstrate a significant reduction in both LDL-C and Lp(a)
concentrations - independent of the concomitant medication - and one of them
reduced plaque size in high risk cardiovascular patients; results of two ongoing
large clinical endpoints studies are awaited. In this review, we summarize and
discuss the recent biological data on PCSK9, the regulation of PCSK9, and finally
briefly summarize the data of recent clinical studies in the context of lipid
metabolism.
|*PCSK9 Inhibitors
[MESH]
|*RNAi Therapeutics
[MESH]
|Animals
[MESH]
|Biomarkers/blood
[MESH]
|Cardiovascular Diseases/*prevention & control
[MESH]
free
free
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