Monocyte and Macrophage Dynamics During Atherogenesis

TL;DR: The pathogenesis of atherosclerosis is discussed with a focus on adaptive immunity and some limitations of animal models and the need for models that are tailored to better translate to human Atherosclerosis and ultimately progress in prevention and treatment are discussed.

TL;DR: The use of mouse models with the ability to turn on or delete proteins or cells in tissue specific and temporal manner will be very valuable as it becomes clear that different factors may influence different stages of lesion development.

TL;DR: The mechanisms of efferocytosis are outlined, from the recognition of dying cells through to phagocytic engulfment and homeostatic resolution, and the pathophysiological consequences that can arise when this process is abrogated are highlighted.

TL;DR: An appreciation of the countervailing mechanisms that modulate inflammation in relation to acute coronary syndromes enriches the fundamental understanding of the pathophysiology of this important manifestation of atherosclerosis and provides glimpses into potential novel therapeutic interventions to forestall this ultimate complication of the disease.

TL;DR: It is concluded that CD36 signaling in response to oxLDL alters cytoskeletal dynamics to enhance macrophage spreading, inhibiting migration and may induce trapping of macrophages in the arterial intima and promote atherosclerosis.

TL;DR: It is shown that the class B scavenger receptor CD36 plays an essential role in macrophage clearance of apoptotic cells in vivo and mass spectrometry analyses of oxPS species identify structures of candidate ligands for CD36 in apoptotic membranes that may facilitate macrophages' recognition.

TL;DR: It is suggested that atherogenesis in human arteries may be linked to Macrophage-induced oxidative modification of LDL mediated by 15-lipoxygenase, leading to subsequent enhanced macrophage uptake, partly by way of the acetyl LDL receptor.

TL;DR: Data indicate that monocytes accumulate continuously during atheroma formation, accumulation increases in proportion to lesion size, and recruitment is augmented with hypercholesterolemia.