Abstract

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.

Highlights

  • 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

  • Studies performed in the last twenty years showed heterogeneous effects of different n-3 n-3 polyunsaturated fatty acids (PUFAs) on various cardiovascular outcomes, which may be of paramount relevance in primary and secondary prevention of cardiovascular disease

  • Recent in vitro investigations as well as clinical studies demonstrated that LC-n3-PUFAs significantly interact with inflammation-related mechanisms, such as endothelial activation, modification of eicosanoid metabolism, and resolution of the inflammatory process

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Summary

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. In the presence of atherosclerosis this balance disrupts leading towards an increase production of proinflammatory cytokines as interleukins 1, 2, and 6 (IL1, 2, and 6) and tumor necrosis factor α (TNF-α), with further progression of the disease [5]. These pro-inflammatory cytokines can induce oxidative stress by enhancing the production of reactive oxygen species (ROS) by monocytes, macrophages, and leukocytes. Plant sources of n-3 fatty acids cannot currently be considered as a replacement for seafood-derived n-3 PUFAs [14] This suggests that n-3 fatty acids derived from different sources might have their own specific effects on cardiovascular risk markers. Derivatives may play a significant role modulating the inflammatory response (Figure 1) [6]

Metabolism of PUFAs
PUFAs and Cardiovascular Disease
PUFAs and Inflammation
Findings
Conclusions
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