Foam cells articles from across Nature Portfolio

Piollet, Porsch et al. report that the myeloid receptor TREM2 limits necrotic core formation in atherosclerosis and controls key atherosclerosis-related functions of macrophages, such as efferocytosis, lipid uptake and foam cell survival.

Specialized pro-resolving mediators (SPM) are involved in the reprogramming of immune responses. Here the authors show that resolvin (RvT) 4 limits the progression of vascular disease in mouse models of arthritis exacerbated atherosclerotic inflammation.

Accumulation of lipid-laden macrophages in the arterial wall is a critical step in atherosclerosis. Here, the authors show that downregulation of Zeb1 in macrophages promotes lipid accumulation and atherosclerotic plaque formation while its restoration with macrophage-targeted nanoparticles reverses these effects.

Patterson, Firulyova, et al. report that TREM2 is a key regulator of foamy macrophage differentiation. Myeloid-specific deletion of Trem2 caused increased macrophage susceptibility to cholesterol-mediated toxicity and cell death and significantly attenuated atherosclerotic plaque progression in mice.

Macrophages have been shown to have an important function in atherosclerosis. Here the authors show that, in human atherosclerotic plaques and mouse models, GSDME and pyroptosis promote atherosclerosis and inhibition of these pathways could reduce pathology associated with atherosclerotic disease.

TREM2 was recently found to have crucial roles in microglia and adipose tissue macrophage function. Research now shows that genetic deletion of macrophage TREM2 modulates lipid uptake, cell death susceptibility and efferocytosis and ultimately reduces experimental atherosclerosis development.

Gwendalyn Randolph describes a 1981 paper by Ross Gerrity that stimulated her career focus on the trafficking of mononuclear phagocytes.