Atherosclerosis
Applied
Type
AdditionConfidence
85%
Created
Mar 27, 2026
Evidence
1 source
Rationale
The existing text focuses exclusively on the cellular mechanisms of atherosclerosis. Integrating the 2025 meta-analysis by Basios et al. provides a necessary clinical bridge, highlighting that while the biological role of LDL is well-understood, the primary therapeutic intervention (statins) faces significant adherence challenges in practice. The abbreviation LDL was expanded to meet the style requirements.
Evidence
Content Changes
removedadded
Endothelial dysfunction allows LDLlow-density lipoprotein (LDL) to penetrate the intima, where it undergoes oxidation. Monocytes adhere, migrate, and differentiate into macrophages, forming foam cells. Smooth muscle proliferation and extracellular matrix deposition lead to fibrous cap formation. Plaque rupture triggers platelet activation and thrombus formation, which can result in acute ischemic events [@libby2021]. Given the central role of LDL in this process, lipid-lowering therapy is foundational to management, although real-world adherence to statin therapy remains a significant clinical challenge influenced by various patient and provider determinants [@basios2025].