AI Article Synopsis

  • * Recent studies reveal that the APOE gene also plays a significant role in Lp(a) levels, especially where the apoE2 variant is concerned, showing that carriers of this variant have lower Lp(a) concentrations.
  • * While the apoE2 genotype can lead to another lipid disorder called dysbetalipoproteinemia, it does not affect Lp(a) levels, indicating that there are complex mechanisms involved in Lp(a) production and metabolism.

Article Abstract

Purpose Of Review: Lipoprotein (a) [Lp(a)] is a highly atherogenic lipoprotein species. A unique feature of Lp(a) is the strong genetic determination of its concentration. The LPA gene is responsible for up to 90% of the variance in Lp(a), but other genes also have an impact.

Recent Findings: Genome-wide associations studies indicate that the APOE gene, encoding apolipoprotein E (apoE), is the second most important locus modulating Lp(a) concentrations. Population studies clearly show that carriers of the apoE2 variant (ε2) display reduced Lp(a) levels, the lowest concentrations being observed in ε2/ε2 homozygotes. This genotype can lead predisposed adults to develop dysbetalipoproteinemia, a lipid disorder characterized by sharp elevations in cholesterol and triglycerides. However, dysbetalipoproteinemia does not significantly modulate circulating Lp(a). Mechanistically, apoE appears to impair the production but not the catabolism of Lp(a). These observations underline the complexity of Lp(a) metabolism and provide key insights into the pathways governing Lp(a) synthesis and secretion.

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Source
http://dx.doi.org/10.1007/s11883-022-01016-8DOI Listing

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