Pathophysiology of hypertriglyceridemia

H. C. Hassing, R. P. Surendran, H. L. Mooij, E. S. Stroes, M. Nieuwdorp, G. M. Dallinga-Thie

Research output: Contribution to journalReview articleAcademicpeer-review

57 Citations (Scopus)

Abstract

The importance of triglycerides as risk factor for CVD is currently under debate. The international guidelines do not include TG into their risk calculator despite the recent observations that plasma TG is an independent risk factor for CVD. The understanding of the pathophysiology of triglycerides opens up avenues for development of new drug targets. Hypertriglyceridemia occurs through I. Abnormalities in hepatic VLDL production, and intestinal chylomicron synthesis 2. Dysfunctional LPL-mediated lipolysis or 3. Impaired remnant clearance. The current review will discuss new aspects in lipolysis by discussing the role of GPIHBP1 and the involvement of apolipoproteins and in the process of hepatic remnant clearance with a focus upon the role of heparin sulfate proteoglycans. Finally we will shortly discuss future perspectives for novel therapies aiming at improving triglyceride homeostasis. This article is part of a Special Issue entitled Triglyceride Metabolism and Disease. (C) 2011 Elsevier B.V. All rights reserved
Original languageEnglish
Pages (from-to)826-832
JournalBIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
Volume1821
Issue number5
DOIs
Publication statusPublished - 2012

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