期刊
BLOOD
卷 127, 期 10, 页码 1221-1222出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2016-01-689034
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- NHLBI NIH HHS [R01 HL077213, P01 HL073311, R01 HL071625] Funding Source: Medline
The importance of research focused on the final events of atherothrombosis cannot be overestimated. Platelet hyperreactivity leading to thrombosis is the main reason for mortality and morbidity in patients with cardiovascular disease and stroke, which together remain a leading cause of death in developed countries. In this issue of Blood, Shen et al(1) establish another functional link between proatherogenic lipoproteins and platelet-mediated thrombus formation with a specific focus on stroke. In their model, the initiating component is L5, the electronegative subfraction of low-density lipoproteins (LDLs), which was shown to be substantially elevated in patients with ischemic stroke. L5 was shown to activate platelets via its receptor, lectin-like oxidized LDL receptor-1 (LOX-1), and ab amyloid peptide, which together contribute to platelet hyperreactivity and stroke complications.
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