Atheroprone flow activates inflammation via endothelial ATP-dependent P2X7-p38 signalling

ConclusionsThese findings reveal that P2X7 is regulated by shear forces leading to its accumulation at atheroprone sites that are exposed to disturbed patterns of blood flow. P2X7 promotes endothelial inflammation at atheroprone sites by transducing ATP signals into p38 activation. Thus P2X7 integrates vascular mechanical responses with purinergic signalling to promote endothelial dysfunction and may provide an attractive potential therapeutic target to prevent or reduce atherosclerosis.
Source: Cardiovascular Research - Category: Cardiology Source Type: research