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Cited by 110

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PCSK9 as a therapeutic target of dyslipidemia

Seidah, Nabil G·2009·Expert Opinion on Therapeutic Targets
DOI 10.1517/14728220802600715
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Abstract

Background Proprotein convertase subtilisin/kexin type 9 (PCSK9), which promotes degradation of hepatic low density lipoprotein receptor (LDLR), has a role in plasma cholesterol metabolism. Its gene is associated with the development of familial hypercholesterolemia. mRNA silencing or inhibition of PCSK9-induced degradation of LDLR may be used to treat this disease. Objective/methods To summarize approaches proposed to reduce the levels of PCSK9 and/or its activity. Results/conclusions mRNA knockdown approaches include the use of antisense oligonucleotides either as soluble phosphorothioates or locked nucleic acids and lipidoid nanoparticles embedded with small interfering RNAs. Passive immunization is also an option. Other strategies include inhibition of the zymogen activation of proPCSK9, or the interaction of PCSK9 with the EGF-A domain of the LDLR. The N-terminal prosegment and the C-terminal Cys-His rich domain (CHRD), are alternative targets. Annexin A2 specifically binds the CHRD and inhibits PCSK9 function, and Annexin A2 peptide mimics could pave the way for the development of novel PCSK9-inhibitory compounds.

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Metadata

Authors
Seidah, N. G.
Venue
Expert Opinion on Therapeutic Targets
Publisher
Informa Healthcare
Published
2008-11-21
Volume
13
Issue
1
Pages
19-28
ISSN
  • 1472-8222
  • 1744-7631
DOI
10.1517/14728220802600715
Cited by
110
References
4
Language
en

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