Phospholipids play an essential role in cell membrane structure and function. The length and number of double bonds of fatty acids in membrane phospholipids are main determinants of fluidity, transport systems, activity of membrane-bound enzymes, and susceptibility to lipid peroxidation. The fatty acid profile of serum lipids, especially the phospholipids, reflects the fatty acid composition of cell membranes. Moreover, long-chain n-3 polyunsatured fatty acids decrease very-low-density lipoprotein assembly and secretion reducing triacylglycerol production. N-6 and n-3 polyunsatured fatty acids are the precursors of signalling molecules, termed “eicosanoids,” which play an important role in the regulation of inflammation. Eicosanoids derived from n-6 polyunsatured fatty acids have proinflammatory actions, while eicosanoids derived from n-3 polyunsatured fatty acids have anti-inflammatory ones. Previous studies showed that inflammation contributes to both the onset and progression of atherosclerosis: actually, atherosclerosis is predominantly a chronic low-grade inflammatory disease of the vessel wall. Several studies suggested the relationship between long-chain n-3 polyunsaturated fatty acids and inflammation, showing that fatty acids may decrease endothelial activation and affect eicosanoid metabolism. 1. Introduction Cardiovascular disease is the leading cause of mortality in many economically developed nations accounting for about 30% of all deaths [1] and its incidence is still increasing. Ongoing research aims to investigate and prevent the early development of cardiovascular risk factors such as atherosclerosis, hypertension, dyslipidemia, chronic inflammation, and insulin resistance. The beneficial effects of n-3 polyunsaturated fatty acids (n-3 PUFAs) were proved in several observational and experimental studies. The lipid lowering action of n3-PUFAs was detected at the beginning, so these nutrients were used for the treatment of dyslipidemic disorders. Their anti-inflammatory, antithrombotic, antiatherosclerotic, and antiarrhythmogenic effects were observed later. Low-grade chronic inflammation is now recognized as a prominent process in the development of atherosclerosis and coronary heart disease. The induction of inflammation may well provide a link between hyperlipidemia and atherogenesis [2, 3]. Atherosclerosis is now considered a “systemic disease” featured by low-grade arterial inflammatory lesions that can develop through the disease progression [4]. In physiological conditions, endothelial cells synthesize and release adequate amounts
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