作者: Yukako Kayashima , Nobuyo Maeda-Smithies
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摘要: Atherosclerosis in different vascular locations leads to distinct clinical consequences, such as ischemic stroke and myocardial infarction. Genome-wide association studies humans revealed that genetic loci responsible for carotid plaque coronary artery disease were not overlapping, suggesting pathways might be involved each location. While elevated plasma cholesterol is a common risk factor, development beds influenced by hemodynamics intrinsic integrity. Despite the limitation of species differences, mouse models provide platforms unbiased approaches. Mouse strain differences also indicate susceptibility atherosclerosis varies, depending on locations, location specificity genetically controlled. Quantitative trait analyses mice suggested candidate genes, including Mertk Stab2, although how gene affects location-specific needs further elucidation. Another approach single-cell transcriptome presence small subpopulation smooth muscle cells (VSMCs), which are “hyper-responsive” inflammatory stimuli. These likely previously-reported Sca1+ progenitor cells, can differentiate into multiple lineages plaques. Further spatiotemporal necessary, since their distribution pattern associated with location-dependent development.