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Cholesteryl Ester Transfer Protein Deficiency and Hyperalphalipoproteinemia.

Akihiro Inazu1

  • 1Department of Clinical Laboratory Science, Graduate School of Medical Science, Kanazawa University.

Journal of Atherosclerosis and Thrombosis
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Summary

Cholesteryl ester transfer protein (CETP) deficiency is linked to lower atherosclerotic cardiovascular disease (ASCVD) risk. However, the connection between very high HDL cholesterol, ASCVD, and age-related macular degeneration (ARMD) requires further investigation.

Keywords:
Age-related macular degeneration (ARMD)ApoC3-rich HDLApoE-rich HDLAtherosclerotic cardiovascular disease (ASCVD)Cholesteryl ester transfer protein (CETP)Coronary artery disease (CAD)D459G variantHDL-TGHyperalphalipoproteinemia (HALP)Lipoprotein(a) [Lp(a)]Major cardiovascular event (MACE)Proprotein convertase subtilisin/kexin 9 (PCSK9)Retinal pigment epithelium (RPE)Small dense LDL (sdLDL)

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Area of Science:

  • Cardiovascular Science
  • Lipid Metabolism
  • Ophthalmology

Background:

  • Cholesteryl ester transfer protein (CETP) plays a crucial role in lipoprotein metabolism.
  • CETP deficiency and CETP inhibitors influence high-density lipoprotein (HDL) cholesterol levels.
  • Associations between lipid profiles, atherosclerotic cardiovascular disease (ASCVD), and age-related macular degeneration (ARMD) are under investigation.

Purpose of the Study:

  • To compare lipoprotein phenotypes in CETP deficiency versus CETP inhibitor use.
  • To summarize and discuss the effects of CETP modulation on ASCVD and ARMD risks.
  • To explore the implications of extremely high HDL cholesterol levels.

Main Methods:

  • Literature review and summary of existing studies on CETP deficiency and inhibitors.
  • Analysis of data regarding ASCVD prevalence in CETP deficiency variants (heterozygotes and homozygotes).
  • Discussion of multifactorial hyperalphalipoproteinemia and its association with ARMD.

Main Results:

  • CETP deficiency, particularly in heterozygotes with truncated variants, is associated with reduced low-density lipoprotein cholesterol and decreased ASCVD risk.
  • ASCVD prevalence was not elevated in individuals with complete CETP deficiency (homozygotes).
  • The etiological basis for the association between ASCVD and ARMD in cases of very high HDL cholesterol needs clarification.

Conclusions:

  • CETP deficiency confers a degree of protection against ASCVD.
  • The link between extremely high HDL cholesterol, ASCVD, and ARMD in multifactorial hyperalphalipoproteinemia warrants further etiological research.
  • Challenges in CETP inhibitor development, including recent findings on obicetrapib, are highlighted.