Key result
Only specific genetic mechanisms regulating triglyceride-rich lipoproteins contribute to CVD risk, revealing new therapeutic targets.
Why the study?
The reliance on triglycerides or triglyceride-rich lipoproteins as cardiovascular disease risk biomarkers prompted investigations into triglyceride-lowering therapies to reduce cardiovascular events.
This review highlights that specific genetic mechanisms regulating triglyceride-rich lipoproteins are causally linked to cardiovascular disease risk, offering new therapeutic targets.
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“Our approach to patients with mild to moderate hypertriglyceridemia (fasting triglycerides ≥150 mg/dL to <880 mg/dL) involves a low fat and low glycemic index diet with caloric restriction in overweight patients, regular exercise, including aerobic and muscle strengthening, and guideline-directed management of major cardiovascular risk factors including intensive control of dysglycemia”
“how you alter the plasma triglyceride-rich lipoproteins (TRLs)”
“This is great science and important research that sheds light on the genetic regulation of TG-rich lipoproteins, serum TG levels, and CVD risk. Since it is hard, if not impossible, to disconnect TG-rich lipoproteins from LDL, we should be humble in extrapolating these findings to clinical medicine in an era of low LDL due to statins and PCSK9 inhibitors. I hope this research identifies new targets for drug therapy and better understanding of CVD risk prediction– only time will tell.”
Advises caution assuming all TRL-lowering mechanisms reduce events; leaves open selective genetic targets for future therapies.
Triglycerides represent 1 component of a heterogeneous pool of triglyceride-rich lipoproteins (TGRLs). The reliance on triglycerides or TGRLs as cardiovascular disease (CVD) risk biomarkers prompted investigations into therapies that lower plasma triglycerides as a means to reduce CVD events. Genetic studies identified TGRL components and pathways involved in their synthesis and metabolism. We advocate that only a subset of genetic mechanisms regulating TGRLs contribute to the risk of CVD events. This "omic" approach recently resulted in new targets for reducing CVD events.
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Rosenson et al. (2014) conducted a review in Atherosclerotic Cardiovascular Disease. Genetic studies indicate that only a subset of genetic mechanisms regulating triglyceride-rich lipoproteins contribute to the risk of cardiovascular disease events, revealing new therapeutic targets.
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