TLR5型
鞭毛蛋白
TLR4型
炎症
Toll样受体
TLR2型
心肌梗塞
医学
病理生理学
受体
体内
免疫学
生物
细胞生物学
心脏病学
先天免疫系统
内科学
遗传学
作者
Roumen Parapanov,Jérôme Lugrin,Nathalie Rosenblatt‐Velin,Bernard Waeber,F. Feihl,Lucas Liaudet
标识
DOI:10.1093/cvr/cvu098.47
摘要
Background: Inflammatory processes play a key role in the pathophysiology of myocardial infarction (MI). Genetic deletion of toll-like recpetors (TLRs), especially TLR2 and TLR4 have shown protective role in murine models of MI. The role of other TLRs remains unknown. We have previously shown that cardiomyocytes express TLR5 and that the ligand of TLR5, flagellin, activates the NF-kappaB and MAPK pathways in cardiomyocytes. We also have shown that injection of flagellin induces acute systolic dysfunction in vivo in mice.
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