期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 124, 期 4, 页码 1462-1465出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI75238
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资金
- NHLBI NIH HHS [R01 HL114567, HL115467-01] Funding Source: Medline
Thromboinflammatory diseases result from the interactions of vascular endothelial cells, inflammatory cells, and platelets with cellular adhesion molecules, plasma proteins, and lipids. Tipping the balance toward a prothrombotic, proinflammatory phenotype results from multicellular activation signals. In this issue of the JCI, Li et al. explore the regulation of heterotypic neutrophil-platelet contacts in response to TNF-alpha-induced venular inflammation with relevance to sickle cell disease (SCD).
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