Publications by authors named "R L Deaton"
Background: Thromboembolic events, including myocardial infarction (MI) or stroke, caused by the rupture or erosion of unstable atherosclerotic plaques are the leading cause of death worldwide. Although most mouse models of atherosclerosis develop lesions in the aorta and carotid arteries, they do not develop advanced coronary artery lesions. Moreover, they do not undergo spontaneous plaque rupture with MI and stroke or do so at such a low frequency that they are not viable experimental models to study late-stage thrombotic events or to identify novel therapeutic approaches for treating atherosclerotic disease.
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- Thromboembolic events from advanced atherosclerosis are the main cause of death globally, and lowering lipids through diet and medication is crucial to reduce cardiovascular risks like heart attacks and strokes.
- Researchers fed mice a high-cholesterol diet followed by a zero-cholesterol diet to study the effects of IL-1β treatment on atherosclerotic lesions, using advanced techniques for analysis.
- While lowering lipids improved several health indicators in mice, IL-1β treatment unexpectedly worsened plaque conditions and increased lesion size, indicating a potential risk with this therapy after diet changes.
Article Synopsis
- Thromboembolic events from advanced atherosclerosis are a major global health issue, and aggressive lipid lowering through diet and drugs is essential to prevent cardiovascular events like heart attacks and strokes.
- A study was conducted using mice to evaluate the impact of switching from a high-fat diet to a low-fat diet on atherosclerotic lesions, involving advanced techniques to analyze lesion characteristics and stability.
- While switching to a low-fat diet significantly lowered LDL cholesterol and improved some aspects of plaque conditions, the addition of an IL-1β antibody treatment unexpectedly worsened the condition by increasing plaque size and cholesterol accumulation.