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Abstract
Many chronic inflammatory processes are linked with the continuous release of inflammatory mediators and the activation of harmful signal-transduction pathways that are able to facilitate disease progression. In this context atherosclerosis represents the most common pathological substrate of coronary heart disease, and the characterization of the disease as a chronic low-grade inflammatory condition is now validated. The biomarkers of inflammation associated with clinical cardiovascular risk support the theory that targeted anti-inflammatory treatment appears to be a promising strategy in reducing residual cardiovascular risk. Several literature data highlight cardioprotective effects of the long-chain omega-3 polyunsaturated fatty acids (PUFAs), such as eicosapentaenoic acid (EPA). This PUFA lowers plasma triglyceride levels and has potential beneficial effects on atherosclerotic plaques. Preclinical studies reported that EPA reduces both pro-inflammatory cytokines and chemokines levels. Clinical studies in patients with coronary artery disease that receive pharmacological statin therapy suggest that EPA may decrease plaque vulnerability preventing plaque progression. This review aims to provide an overview of the links between inflammation and cardiovascular risk factors, importantly focusing on the role of diet, in particular examining the proposed role of EPA as well as the success or failure of standard pharmacological therapy for cardiovascular diseases.
Highlights
Role of eicosapentaenoic acid (EPA) in Inflammation: Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Formation and rupture of atherosclerotic plaque are closely connected with the development of the inflammatory process. The lipoprotein stimulates both chemokines and endothelial cells that facilitate the recruitment of lymphocytes and adherent monocytes to the forming lesion site; growth factors and cytokines formed by the inflammatory intima stimulate the differentiation of monocytes into macrophages linked by the upregulation of the TLRs, in particular TLR4 and scavenger receptors; the macrophages activated form foam-like cells or stimulate an inflammatory cascade that lead to atherosclerotic plaque formation [9]
Numerous studies have shown that the inflammatory process is the basis of various diseases; in this context, it is recognized that the role of fatty acids is to control inflammation by changing their composition in cell membranes, for example making it more fluid or altering its gene expression
Summary
Inflammation is classified as “normal defense mechanism” able to preserve the host from both infections and insults; the involvement of the inflammatory process helps to restore homeostasis at damaged or infected sites. Literature data have reported, that several chronic inflammatory processes are linked with the continuous release of inflammatory mediators and the activation of harmful signal-transduction pathway that facilitate disease progression In these cases, there are high concentrations of inflammatory markers and cells both at the primary site of damage and at the systemic level, as occurs in cardiovascular disease or rheumatoid arthritis. Mast cells have been implicated in the pathophysiology of many diseases, including allergy, asthma, anaphylaxis, gastrointestinal disorders, many types of malignancies, and cardiovascular diseases The characteristic of these cells is to undergo a degranulation process when activated by tissue damage; proinflammatory molecules are released from the granules such as histamine, tumor necrosis factor (TNF), kinin, and leukotrienes [4]
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