Modulation of platelet function with dietary polyphenols
A promising strategy in the prevention of cardiovascular disease
Beyond being central players in haemostasis and thrombosis, platelets have crucial roles in the development of atherosclerosis, mediated through their interactions with monocytes and endothelial cells. Disturbed platelet function correlates with other risk factors and the progression of CVD, postulating platelets as rational targets in CVD prevention. The effects of polyphenols on platelets have been studied in numerous pre-clinical and clinical trials, and the data reported from these studies support the hypothesis that modulation of platelet function contributes significantly to pleiotropic beneficial effects of polyphenols on cardiovascular health. To provide comprehensive scientific evidence for the promotion of polyphenols as antiplatelet agents, further studies should address the influence of polyphenol metabolism on the observed effects, identify active polyphenols/metabolites and elucidate the precise mechanisms of their action.
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in Europe. According to the last available data it is responsible for 46% of overall mortality and with more than 4 million people that die of CVD every year, it causes more than twice as many deaths as cancer (1). The underlying cause of the vast majority of cardiovascular events is atherosclerosis, a lifelong systemic pathological process characterized by accumulation of cells, inflammation, fatty deposits and ultimately scarring of the tissue within artery walls. Beyond being central players in haemostasis and thrombosis, platelets have crucial role in the development of atherosclerosis. Thus, platelets are considered an emerging target for the prophylactic effects of food bioactives in CVD with promising scientific evidence of their efficacy.
PLATELETS AND CVD
The involvement of platelets in atherosclerosis and thrombosis is a result of their interaction with other platelets, monocytes, neutrophils and endothelial cells and these interactions occur upon platelet activation which is mediated by various physiological and patho-ph ...