Abstract
Apolipoprotein C-III has been referred to as an important participant in the metabolism of triglyceride-rich lipoproteins, leading to hypertriglyceridemia and thereafter cardiovascular disease. Accumulating evidence indicates that apolipoprotein C-III is a multifaceted protein which not only regulates triglyceride metabolism, but also participates in the atherosclerotic lesion formation and several other pathological processes involved in atherosclerosis. Based on data from experiments and clinical trials, some novel therapies such as antisense technology emerge.
Highlights
Triglyceride (TG) has been identified as an important risk factor for cardiovascular disease (CVD) for a long time, but randomized controlled trials of fenofibrate and omega-3 fatty acids to reduce TG failed to show any significant clinical benefits [1, 2]
Renewed interest in TG is brought by recent genetic observations that loss-of-function (LOF) mutations in the gene encoding apolipoprotein C-III and relevant hypotriglyceremia are associated with decreased CVD risk (40–41 %) [4, 5]
ApoCIII, an apolipoprotein composed of 79 amino acids with a molecular weight of 8.8 kDa, resides on circulating HDL, low density lipoprotein (LDL) and triglyceriderich lipoproteins (TRLs) such as chylomicrons (CM) and very low density lipoprotein (VLDL) [6]
Summary
Triglyceride (TG) has been identified as an important risk factor for cardiovascular disease (CVD) for a long time, but randomized controlled trials of fenofibrate and omega-3 fatty acids to reduce TG failed to show any significant clinical benefits [1, 2]. ApoCIII and the lipoproteins that carry apoCIII acts as a key regulator in the TG metabolism, and an independent predictor for CVD risk [9, 10]. A recent study by Zheng et al extends the experiments from venous endothelium to coronary artery endothelium and provides in vivo evidence for the independent atherogenic effects of apoCIII and atheroprotective effects of statins because of decreasing apoCIII [16].
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call