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dc.contributor.authorNorata, Giuseppe
dc.contributor.authorTsimikas, S.
dc.contributor.authorPirillo, A.
dc.contributor.authorCatapano, A.
dc.date.accessioned2017-08-24T02:23:42Z
dc.date.available2017-08-24T02:23:42Z
dc.date.created2017-08-23T07:21:47Z
dc.date.issued2015
dc.identifier.citationNorata, G. and Tsimikas, S. and Pirillo, A. and Catapano, A. 2015. Apolipoprotein C-III: From Pathophysiology to Pharmacology. Trends in Pharmacological Sciences. 36 (10): pp. 675-687.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/56381
dc.identifier.doi10.1016/j.tips.2015.07.001
dc.description.abstract

© 2015 Elsevier Ltd. All rights reserved. Apolipoprotein C-III (apoC-III) has a critical role in the metabolism of triglyceride (TG)-rich lipoproteins (TRLs). Animal models lacking the APOC3 gene exhibit reduced plasma TG levels, whereas the overexpression of APOC3 leads to increased TG levels. In humans, loss-of-function mutations in APOC3 are associated with reduced plasma TG levels and reduced risk for ischemic vascular disease and coronary heart disease. Several hypolipidemic agents have been shown to reduce apoC-III, including fibrates and statins, and antisense technology aimed at inhibiting APOC3 mRNA to decrease the production of apoC-III is currently in Phase III of clinical development. Here, we review the pathophysiological role of apoC-III in TG metabolism and the evidence supporting this apolipoprotein as an emerging target for hypertriglyceridemia (HTG) and associated cardiovascular disorders.

dc.titleApolipoprotein C-III: From Pathophysiology to Pharmacology
dc.typeJournal Article
dcterms.source.volume36
dcterms.source.number10
dcterms.source.startPage675
dcterms.source.endPage687
dcterms.source.issn0165-6147
dcterms.source.titleTrends in Pharmacological Sciences
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusFulltext not available


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