Fractalkine as an important target of aspirin in the prevention of atherogenesis : Editorial to: 'Aspirin inhibits fractalkine expression in atherosclerotic plaques and reduces atherosclerosis in ApoE gene knockout mice' by H. Liu et al.

摘要

Since its discovery in the 1850s, aspirin, or acetylsalicylic acid, has been widely used as an anti-inflammatory, analgesic and antipyretic drug. In addition, aspirin therapy reduces the incidence of myocardial infarction in patients with a high risk on occlusive vascular events [1], which has been attributed to aspirin's anti-platelet properties. By inhibiting COX activity, low-dose aspirin mainly prevents prothrombotic thromboxane A_2 production in platelets due to their inability to regenerate COX1. This shifts the haemostatic thromboxane-prostacyclin balance and favours the prostacyclin-mediated inhibition of platelet aggregation, thereby reducing the risk of thrombus formation in high-risk patients [2]. Interestingly, aspirin administration has also been reported to reduce the development and progression of atherosclerosis in hyperlipidaemic mice [3-6]. This property goes beyond aspirin's ability to block COX1 activity, as COX1 inhibition can only reduce atherosclerotic plaque formation in early stages, without affecting the progression of established lesions [7]. This emphasizes the importance of COX-independent anti-inflammatory actions of aspirin in its therapeutic value.