Biology, pathophysiology and current therapies that affect lipoprotein (a) levels

Thampi Rawther; Fatiha Tabet

doi:10.1016/j.yjmcc.2019.04.005

Biology, pathophysiology and current therapies that affect lipoprotein (a) levels

J Mol Cell Cardiol. 2019 Jun:131:1-11. doi: 10.1016/j.yjmcc.2019.04.005. Epub 2019 Apr 12.

Authors

Thampi Rawther¹, Fatiha Tabet²

Affiliations

¹ School of Medical Sciences, Faculty of Medicine, UNSW Sydney, Sydney, NSW 2052, Australia.
² School of Medical Sciences, Faculty of Medicine, UNSW Sydney, Sydney, NSW 2052, Australia. Electronic address: fatiha.tabet@yahoo.ca.

PMID: 30986377
DOI: 10.1016/j.yjmcc.2019.04.005

Abstract

Lipoprotein (a) [Lp(a)] has recently emerged as a causal, independent and genetic risk factor for cardiovascular disease and calcific aortic valve disease. Given the high incidence of elevated Lp(a) among the general population, significant gaps in the knowledge of Lp(a) biology, pathophysiology and current therapies affecting Lp(a) reduction exist. As plasma Lp(a) levels are genetically determined and insensible to diet, exercise and lifestyle changes, lipid-lowering therapies seem to be the solution to lower elevated Lp(a) levels. This review summarises the current knowledge of Lp(a) structure, metabolism, catabolism, pathophysiology, and Lp(a) response to statins, lipid apheresis, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, cholesterol esterase transferase protein (CETP) inhibitors and antisense oligonucleotides (ASOs).

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Enzyme Inhibitors / pharmacology
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology
Lipoprotein(a) / blood*

Substances

Enzyme Inhibitors
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Lipoprotein(a)