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dc.contributor.authorTibolla, G.
dc.contributor.authorNorata, Giuseppe
dc.contributor.authorArtali, R.
dc.contributor.authorMeneghetti, F.
dc.contributor.authorCatapano, A.
dc.date.accessioned2017-08-24T02:18:28Z
dc.date.available2017-08-24T02:18:28Z
dc.date.created2017-08-23T07:21:46Z
dc.date.issued2011
dc.identifier.citationTibolla, G. and Norata, G. and Artali, R. and Meneghetti, F. and Catapano, A. 2011. Proprotein convertase subtilisin/kexin type 9 (PCSK9): From structure-function relation to therapeutic inhibition. Nutrition, Metabolism and Cardiovascular Diseases. 21 (11): pp. 835-843.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/55419
dc.identifier.doi10.1016/j.numecd.2011.06.002
dc.description.abstract

Aims: This short review aims at summarizing the current information on Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) structure and function focusing also on the therapeutic possibilities based on the inhibition of this protein. Data synthesis: PCSK9 has been recently discovered as the third gene involved in autosomal dominant hypercholesterolemia. PCSK9 binds and favors degradation of the low-density lipoprotein receptor (LDLR) and thereby modulates the plasma levels of LDL-cholesterol (LDL-C). Some of the natural occurring PCSK9 mutations increase the protein function (gain of function) and cause hypercholesterolemia, whereas loss of function mutations associate with hypocholesterolemia. Since the loss of a functional PCSK9 in humans is not associated with apparent deleterious effects, this protease is an attractive target for the development of lowering plasma LDL-C agents, either alone or in combination with statins. Conclusion: Inhibition of PCSK9 is emerging as a novel strategy for the treatment of hypercholesterolemia and data obtained from pre-clinical studies show that use of monoclonal antibodies, antisense oligonucleotides and short interfering RNA are effective in reducing LDL-C, clinical studies, accompanied by a better understanding of PCSK9 biology, are now necessary to address whether these new compounds will have a future in clinical practice. © 2011 Elsevier B.V.

dc.publisherElsevier
dc.titleProprotein convertase subtilisin/kexin type 9 (PCSK9): From structure-function relation to therapeutic inhibition
dc.typeJournal Article
dcterms.source.volume21
dcterms.source.number11
dcterms.source.startPage835
dcterms.source.endPage843
dcterms.source.issn0939-4753
dcterms.source.titleNutrition, Metabolism and Cardiovascular Diseases
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusFulltext not available


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