Why the study?
Recent evidence indicated that apoC3 and apoA5 play opposite roles in lipid metabolism and CAD risk, warranting a review of existing evidence and their potential correlation.
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Design
Review article
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ApoC3 and apoA5 have opposite effects on triglyceride metabolism and coronary artery disease risk, emerging as potential novel targets for cardiovascular risk reduction.
Apolipoprotein C3 (apoC3) and apolipoprotein A5 (apoA5), encoded by APOA1/C3/A4/A5 gene cluster, are two critical regulators of plasma triglyceride (TG) metabolism. Deficiency of apoC3 or apoA5 led to significant decreased or increased plasma TG levels, respectively. Recent studies indicated apoC3 and apoA5 also played roles in plasma remnant cholesterol, high density lipoprotein (HDL) and hepatic TG metabolisms. Moreover, large scale population genetic studies indicated that loss of function mutations in APOC3 and APOA5 gene conferred decreased and increased risk of coronary artery disease (CAD), respectively. This manuscript mainly reviewed existing evidences suggesting the opposite role of apoC3 and apoA5 in lipid metabolism and CAD risk, and discussed the potential correlation between these two apolipoproteins.
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Dai et al. (2019) studied this question.
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