AbstractPurpose of review
Chronic inflammation and disordered lipid metabolism represent hallmarks of atherosclerosis. Considerable evidence has accumulated to suggest that innate immune defense mechanisms might interact with proinflammatory pathways and exacerbate or perhaps even initiate development of arterial plaques. Until recently the preponderance of such evidence has been indirectly emerging from clinical and epidemiologic studies, with some support from experimental animal models of atherosclerosis.Recent findings
Recent data now directly implicate signaling by toll-like receptor 4 and the common adaptor molecule MyD88 in the pathogenesis of atherosclerosis, establishing a key link between atherosclerosis and defense against both foreign pathogens and endogenously generated inflammatory ligands.Summary
Here we briefly review these and closely related studies, highlighting areas that should provide fertile ground for future studies aimed at a more comprehensive understanding of the interplay between innate immune defense mechanisms, atherosclerosis and related vascular disorders.