Response: Lipoprotein subclass profiling reveals pleiotropy in the genetic variants of lipid risk factors for coronary heart disease: A note on mendelian randomization studies

摘要

We thank Wurtz and colleagues for their positive comments on our recent paper (1) on remnant cholesterol (remnant-C) as a causal risk factor for ischemic heart disease. We naturally agree that lipoprotein metabolism is very complex, with many subclasses of lipoproteins and different lipid contents of these subclasses, making it difficult, if not impossible, to find genetic instruments completely without pleiotropic effects on the other lipoprotein subclasses. The various lipoprotein subclasses derived from the endogenous pathway are a continuum from large very-low-density lipoproteins excreted from the liver, which are then degraded into intermediate-density lipoproteins by lipolysis and exchange of lipids and apoli-poproteins in plasma, which are then degraded further into low-density lipoproteins.