Relevance of platelet-independent effects of aspirin to its salutary effect in atherosclerosis-related events.
There is a close inter-relationship between oxidative stress, coagulation, inflammation, and smooth muscle cell growth as key components of atherosclerosis (Fig. 1). As an analgesic and anti-pyretic, aspirin has been in use for over a century. It acetylates the COX enzyme, irreversibly inhibiting the formation of prostaglandin. Its action on platelet TxA2 has highlighted its role as an anti-thrombotic agent in cardiovascular patients. Over the last two decades, unique anti-inflammatory properties of aspirin not shared by other non-steroidals have been discovered. Aspirin biotransforms into salicylate, which has diverse but potent anti-inflammatory properties. As we strive to better understand the concepts of atherogenesis, chronic inflammation, oxidative stress, and endothelial activation, these novel effects of aspirin provide new insights as to how this wonder drug works. These effects of aspirin alter many, if not all, components of the atherogenesis cascade shown in Fig. 1.
Khan
Qaisar
Q
Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences College of Medicine and the Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA.
Mehta
Jawahar L
JL
D001241:Aspirin / Q000494:pharmacology*; D050197:Atherosclerosis / Q000503:physiopathology*; D002448:Cell Adhesion / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002634:Chemotaxis, Leukocyte / Q000187:drug effects; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D006801:Humans; D007962:Leukocytes / Q000187:drug effects / Q000502:physiology; D032389:Myocytes, Smooth Muscle / Q000187:drug effects / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects*; D012980:Sodium Salicylate / Q000494:pharmacology
D001241:Aspirin; D012980:Sodium Salicylate