期刊
BLOOD
卷 129, 期 11, 页码 1415-1419出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2016-07-692673
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资金
- National Heart, Lung, and Blood Institute of the National Institutes of Health [R01-HL078610, R01-HL111969, R01-HL120046, T32-HL094294, K08-HL133493]
- National Space Biomedical Research Institute [14-14NSBRI10025]
The role of platelet adhesion, activation, and aggregation in acute atherothrombotic events such as myocardial infarction and strokeis wellestablished. Thereis increasing evidence that platelet-endothelial interactions also contribute to early atherosclerotic plaque initiation and growth. Through these interactions, platelet-derived factors can contribute to the proinflammatory and mitogenic status of resident mural cells. Among the many putative mechanisms for platelet-endothelial interactions, increased endothelial-associated von Willebrand factor, particularly in a multimerized form, which interacts with platelet glycoproteins and integrins, is a major factor and represents a therapeutic target in early atherogenesis.
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