Language

English

Publication Date

7-1-2024

Journal

Current Atherosclerosis Reports

DOI

10.1007/s11883-024-01209-3

PMID

38753254

PMCID

PMC11192678

PubMedCentral® Posted Date

5-16-2024

PubMedCentral® Full Text Version

Post-print

Abstract

Purpose of review: Low-density lipoprotein (LDL) poses a risk for atherosclerotic cardiovascular disease (ASCVD). As LDL comprises various subtypes differing in charge, density, and size, understanding their specific impact on ASCVD is crucial. Two highly atherogenic LDL subtypes-electronegative LDL (L5) and Lp(a)-induce vascular cell apoptosis and atherosclerotic changes independent of plasma cholesterol levels, and their mechanisms warrant further investigation. Here, we have compared the roles of L5 and Lp(a) in the development of ASCVD.

Recent findings: Lp(a) tends to accumulate in artery walls, promoting plaque formation and potentially triggering atherosclerosis progression through prothrombotic or antifibrinolytic effects. High Lp(a) levels correlate with calcific aortic stenosis and atherothrombosis risk. L5 can induce endothelial cell apoptosis and increase vascular permeability, inflammation, and atherogenesis, playing a key role in initiating atherosclerosis. Elevated L5 levels in certain high-risk populations may serve as a distinctive predictor of ASCVD. L5 and Lp(a) are both atherogenic lipoproteins contributing to ASCVD through distinct mechanisms. Lp(a) has garnered attention, but equal consideration should be given to L5.

Keywords

Humans, Lipoprotein(a), Atherosclerosis, Lipoproteins, LDL, Apoptosis, Animals, Lp(a), L5, Electronegative LDL, Atherogenesis, Atherosclerotic Cardiovascular Disease, Oxidized LDL

Published Open-Access

yes

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