Mechanisms
Lp(a) drives inflammation, atherosclerosis and thrombosis via oxidised phospholipid transport, but measurement standardisation still lags, a review (Molecules 2023)
Original title: Lipoprotein(a) in Atherosclerotic Diseases: From Pathophysiology to Diagnosis and Treatment
This narrative review summarises the pathophysiology, diagnosis and treatment of Lp(a) in atherosclerotic disease. Lp(a), an LDL-like particle bound to apolipoprotein(a), is a heritable, independent causal risk factor for atherosclerotic cardiovascular disease, largely determined by variation at the LPA gene locus. As the preferential carrier of oxidised phospholipids in plasma, Lp(a) adversely affects vascular inflammation, atherosclerotic lesion development, endothelial function and thrombogenicity. Despite its established pathogenic role, Lp(a) measurement still lacks a globally standardised method, complicating comparisons between laboratories. Standard lipid-lowering therapies, statins, fibrates and ezetimibe, have only a mediocre effect on Lp(a), and whether this translates into altered cardiovascular outcomes remains unclear.
Original abstract
Lipoprotein(a) (Lp(a)) is a low-density lipoprotein (LDL) cholesterol-like particle bound to apolipoprotein(a). Increased Lp(a) levels are an independent, heritable causal risk factor for atherosclerotic cardiovascular disease (ASCVD) as they are largely determined by variations in the Lp(a) gene (LPA) locus encoding apo(a). Lp(a) is the preferential lipoprotein carrier for oxidized phospholipids (OxPL), and its role adversely affects vascular inflammation, atherosclerotic lesions, endothelial function and thrombogenicity, which pathophysiologically leads to cardiovascular (CV) events. Despite this crucial role of Lp(a), its measurement lacks a globally unified method, and, between different laboratories, results need standardization. Standard antilipidemic therapies, such as statins, fibrates and ezetimibe, have a mediocre effect on Lp(a) levels, although it is not yet clear whether such treatments can affect CV events and prognosis. This narrative review aims to summarize knowledge regarding the mechanisms mediating the effect of Lp(a) on inflammation, atherosclerosis and thrombosis and discuss current diagnostic and therapeutic potentials.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.