Publication Date
5-1-2022
Journal
Current Atherosclerosis Reports
DOI
10.1007/s11883-022-01006-w
PMID
35274230
PMCID
PMC9575332
PubMedCentral® Posted Date
10-17-2022
PubMedCentral® Full Text Version
Author MSS
Published Open-Access
yes
Keywords
Atherosclerosis, Humans, Hyperlipidemias, Hypertriglyceridemia, Inflammation, Risk Factors, Triglycerides, Hypertriglyceridemia (HTG), Triglyceride-rich lipoproteins (TGRL), Remnant lipoprotein particles (RLP), Inflammation, Atherosclerotic cardiovascular disease (ASCVD)
Abstract
Purpose of Review
Recent studies indicate an association between hypertriglyceridemia (HTG) and atherosclerotic cardiovascular disease (ASCVD). The purpose of this review is to discuss the potential mechanism connecting HTG and ASCVD risk and the potential efficacy of HTG-targeting therapies in ASCVD prevention.
Recent Findings
HTG, with elevations in triglyceride-rich lipoproteins (TGRL) and their remnants, are causal ASCVD risk factors. The mechanisms whereby HTG increases ASCVD risk are not well understood but may include multiple factors. Inflammation plays a crucial role in atherosclerosis. TGRL compared to low-density lipoproteins (LDL) correlate better with inflammation. TGRL remnants can penetrate endothelium and interact with macrophages leading to foam cell formation and inflammation in arterial walls, thereby contributing to atherogenesis. In addition, circulating monocytes can take up TGRL and become lipid-laden foamy monocytes, which infiltrate the arterial wall and may also contribute to atherogenesis. Novel therapies targeting HTG or inflammation are in development and have potential of reducing residual ASCVD risk associated with HTG.
Summary
Clinical and preclinical studies show a causal role of HTG in promoting ASCVD, in which inflammation plays a vital role. Novel therapies targeting HTG or inflammation have potential of reducing residual ASCVD risk.