Macrophages, lipid metabolism and gene expression in atherogenesis: a therapeutic target of the future?

Absract

Cardiovascular disease results in more deaths globally than any other ailment. A major contributing factor to its pathology is atherosclerosis; an inflammatory disorder characterized by the development of fibrotic plaques within the arterial walls. Key to the progression of atherosclerosis are macrophages that contribute to plaque development by transforming into lipid-loaded foam cells upon internalization of modified lipoproteins. Accumulation of such foam cells in the arterial wall initiates the formation of fatty streaks that subsequently develop into advanced plaques that are prone to rupture. Clearly, macrophage lipid metabolism and foam cell biology represent a key avenue of research during the ongoing search for novel therapeutic targets that can be used in the clinical intervention of atherosclerosis. In this article, we aim to summarize the current status of research on macrophages, lipid metabolism and gene expression in relation to atherogenesis and both current and potential future therapies.

Key Words:

• anti-inflammatory therapy
• atherosclerosis
• cholesterol
• foam cell
• macrophage
• nuclear receptor agonist
• statin