The Cellular Biology of Macrophages in Atherosclerosis

By K. Moore, I. Tabas. Cell, 2011

2,598 citations recorded by the source corpus.

Macrophages are becoming increasingly recognized as key agents in chronic diseases of aging, including cancer, metabolic disease, and, the topic of this review, atherosclerosis. In atherosclerosis, monocytes hone to focal area of the arterial subendothelium in response to matrix-retained apolipoprotein B-lipoproteins. Monocyte-derived macrophages then participate in a maladaptive, non-resolving inflammatory response that leads to subendothelial expansion with additional cells, lipid, and matrix. A few lesions undergo necrotic disruption, triggering acute thrombotic vascular disease, including myocardial infarction, stroke, and sudden cardiac death. This review discusses how macrophages contribute to both early and advanced atherosclerosis, with an emphasis on concepts supported by solid mechanistic and in-vivo data.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/099abbaa63247cd29b3fa8bdd3157f3d7e126e88

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Citations in the corpus

Insulin Resistance, Hyperglycemia, and Atherosclerosis (2011, positive): “Macrophages Monocyte-derived macrophages play critical roles in all stages of atherosclerosis (Moore and Tabas, 2011).”
Macrophage phenotypes in atherosclerosis (2014, background): “fibrosis by selectively stimulating and activating transforming growth factor beta(1).”
Macrophage Autophagy Plays a Protective Role in Advanced Atherosclerosis (2012, background): “In vivo data suggest that endoplasmic reticulum (ER) and oxidative stress play important roles C in advanced lesional macrophage death (Lusis, 2000; Moore and Tabas, 2011).”
Macrophage Polarization in Inflammatory Diseases (2014, background): “Atherosclerosis is a common type of degenerative disease of the vessel wall characterized by the accumulation of apolipoprotein B-lipoproteins in the inner lining of large and medium sized arteries [41].”
Oxidized Low-Density Lipoprotein Induces Long-Term Proinflammatory Cytokine Production and Foam Cell Formation via Epigenetic Reprogramming of Monocytes (2014, background): “to the generation of foam cells, thereby contributing to the formation of atherosclerotic plaques.(6) Therefore, we explored”