DOI: 10.2337/DB14-1963
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摘要: The risk of cardiovascular events in humans increases the presence type 1 or 2 diabetes mellitus, large part due to exacerbated atherosclerosis. Genetically engineered mouse models have begun elucidate cellular and molecular mechanisms responsible for diabetes-exacerbated Research on these has revealed that independently accelerates initiation progression lesions atherosclerosis also impairs regression following aggressive lipid lowering. Myeloid cell activation combination with proatherogenic changes allowing increased monocyte recruitment into arteries diabetic mice emerged as an important mediator effects three stages appear be dependent interplay between glucose lipids, well other factors, result monocytes both progressing regressing Importantly, some by are now being studied human subjects. This Perspective highlights new mechanistic findings based discusses relevance areas which more research is urgently needed order lessen burden macrovascular complications mellitus.