Apoprotein C-III: A review of its clinical implications

• ApoproteinC-III (apoC-III) has a validated link with hypertriglyceridemia and cardiovascular disease (CVD) in human.
• ApoC-III exerts its atherogenic effect by means of not only causing lipid metabolism dysfunction but also accelerating pro-inflammatory process.
• ApoC-III correlates closely with diabetes in its apoptosis process of islet β cells and has relevance with other diseases for its gene mutations.
• New antisense drug targeting specifically on apoC-III mRNA can hopefully reduce the CVD risk caused by plasma apoC-III.

Apoprotein C-III (apoC-III), originating from the apoA-I/C-III/A-IV gene cluster affected by multiple regulating factors, has been demonstrated to have a validated link with hypertriglyceridemia in humans. Following genome studies establishing the impact of apoC-III on both plasma triglyceride (TG) level and cardiovascular disease (CVD), apoC-III offers us a novel explanation attempting to resolve the long-existing confusion with regard to the atherogenic effect of TG. Notably, apoC-III exerts its atherogenic effect by means of not only intervening in the function and metabolism of various lipid molecules, but also accelerating pro-inflammatory effects between monocytes and endothelial cells. Data have suggested that diabetes, a common endocrine disease, also correlates closely with apoC-III in its apoptosis process of islet βcells. In fact, apoC-III genes, with various mutations among individuals, are also found to have relevance to other diseases, including fatty liver disease. Fortunately, besides present day therapeutic strategies, such as lifestyle changes and lipid-lowering drug treatments, a promising new antisense drug specifically targeting on apoC-III gene expression opens up new avenues. This article mainly summarizes the clinical implication of apoC-III and its future directions of treatment.