Key result
Apolipoprotein C-III represents a promising therapeutic target for atherosclerosis, with targeted therapies effectively lowering triglycerides, though their direct impact on atherosclerotic plaque reduction requires long-term clinical trials.
Why the study?
The broader implications of apolipoprotein C-III in the pathogenesis of atherosclerosis remain to be fully elucidated.
This review highlights apoC-III as a critical multifaceted factor in atherosclerosis beyond just triglyceride regulation, underscoring the urgent need for dedicated cardiovascular outcome trials to validate the clinical benefit of novel apoC-III-targeted therapies.
Apolipoprotein C-III (apoC-III) has emerged as a pivotal therapeutic target for lipid-lowering therapies, particularly for hypertriglyceridemia. However, its broader implications in the pathogenesis of atherosclerosis remain to be fully elucidated. ApoC-III is extensively studied for its classical role in modulating lipoprotein lipase activity; nevertheless, recent evidence highlights its multifaceted mechanisms involving the regulation of remnant cholesterol clearance, low-density lipoprotein subfraction transformation, high-density lipoprotein functionality, and inflammasome activation. Meanwhile, the emergence of novel APOC3 gene-edited models beyond murine systems has provided indispensable perspectives for deciphering the complex links between apoC-III and atherogenesis. Therefore, this review aims to comprehensively summarize the translational research surrounding apoC-III, from its central function in lipoprotein metabolism to its critical lipoprotein lipase-independent effects, offering a promising outlook for the clinical management of atherosclerotic cardiovascular disease.
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Yang et al. (2026) conducted a review in Atherosclerosis and Hypertriglyceridemia. Apolipoprotein C-III targeted therapies was evaluated. Apolipoprotein C-III represents a promising therapeutic target for atherosclerosis, with targeted therapies effectively lowering triglycerides, though their direct impact on atherosclerotic plaque reduction requires long-term clinical trials.
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