The iterative lipid impact on inflammation in atherosclerosis

Area of Science:

• Cardiovascular Biology
• Immunology
• Atherosclerosis Research

Background:

• Atherogenesis is characterized by chronic inflammation.
• Key lipoproteins, including low-density lipoprotein cholesterol (LDL-C), triglyceride-rich lipoproteins (TRLs), and lipoprotein(a) [Lp(a)], are causally linked to atherosclerosis.
• These lipoproteins trigger pro-inflammatory pathways within the artery wall.

Purpose of the Study:

• To review the multifaceted effects of lipoproteins on systemic inflammatory pathways in the context of atherosclerosis.
• To highlight the role of lipoproteins in endothelial activation and lipid deposition.
• To explore the connection between lipid metabolism and inflammatory responses in cardiovascular disease.

Main Methods:

• This is a review article, synthesizing existing research.
• The review focuses on the mechanistic links between lipoproteins and inflammation.
• Key findings from studies on endothelial dysfunction, immune cell activation, and trained immunity are discussed.

Main Results:

• Apolipoprotein B-containing lipoproteins induce pro-inflammatory effects both locally in the artery and systemically.
• LDL-C, TRLs, and Lp(a) contribute to endothelial dysfunction and monocyte activation via lipid accumulation.
• LDL-C is a significant inducer of trained immunity, propagating low-grade inflammation and myeloid-biased bone marrow activation, which mobilizes immune cells and advances plaque progression.

Conclusions:

• Lipoproteins and inflammation are intrinsically linked in the development of atherosclerosis.
• Further elucidation of these inflammatory pathways offers potential targets for novel therapeutic interventions.
• Targeting lipoprotein-driven inflammation may provide new strategies for managing cardiovascular disease.