[Atherogenic modification of low-density lipoproteins]

Area of Science:

• Cardiovascular Biology
• Atherosclerosis Pathogenesis
• Lipoprotein Metabolism

Background:

• Atherosclerosis initiation involves cholesterol ester accumulation in arterial intima.
• Foam cell formation is a critical trigger in atherosclerotic pathogenesis.
• Circulating low-density lipoprotein (LDL) is the primary source of arterial lipids.

Purpose of the Study:

• To review the features and atherogenic role of various modified LDL forms.
• To highlight the significance of desialylated and multiple-modified LDL in atherogenesis.

Main Methods:

• Review of existing literature on LDL modifications and their impact on atherosclerosis.
• Analysis of cellular and molecular mechanisms underlying LDL-induced atherogenesis.

Main Results:

• Multiple modified LDL forms, including oxidized, small dense, electronegative, and desialylated LDL, are implicated in atherogenesis.
• Desialylated LDL actively induces lipid accumulation in cultured cells, confirming its atherogenic potential.
• Naturally occurring multiple-modified LDL stimulates intracellular lipid accumulation, cell proliferation, and fibrosis, contributing to atherosclerotic lesion development.

Conclusions:

• Multiple modifications of LDL particles in plasma represent a cascade of changes promoting atherosclerosis.
• Desialylated and other multiple-modified LDL forms are significant contributors to the pathogenesis of atherosclerotic lesions.