Why the study?
Despite achieving recommended LDL-C targets, many patients remain at high risk of cardiovascular events due to elevated triglyceride-rich lipoproteins and remnants.
ANGPTL3 inhibition represents a promising therapeutic strategy for addressing residual cardiovascular risk by improving lipid profiles independent of LDL receptor function.
Supports ANGPTL3 inhibition for apolipoprotein B reduction beyond LDL receptor pathways; leaves open cardiovascular outcome confirmation in trials.
Despite achieving recommended low-density lipoprotein cholesterol (LDL-C) targets, many patients remain at high risk of cardiovascular events due to elevated triglyceride-rich lipoproteins and remnants. Angiopoietin-like protein 3 (ANGPTL3) has emerged as a promising therapeutic target for addressing this residual risk. As a liver-secreted regulator of lipoprotein metabolism, ANGPTL3 influences triglycerides, LDL-C, and high-density lipoprotein cholesterol through inhibition of lipoprotein lipase and endothelial lipase. Human genetic studies and pharmacologic interventions consistently show that ANGPTL3 inhibition improves lipid profiles and lowers apolipoprotein B-containing lipoproteins, independent of LDL receptor function. This review integrates biological, genetic, and clinical evidence, and provides an overview of novel ANGPTL3-targeted therapies, offering new perspectives for cardiovascular prevention and lipid management.
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Weng et al. (2026) studied this question.
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