Inflammation and Genetics of Inflammation in Cardiovascular Diseases

Abstract

Inflammation is a complex of defensive mechanisms reacting to the entry of harmful agents to the organism or cells in order to eliminate or at least to dilute the agent, repair damaged cells or tissue and restore homeostasis. From this definition it is clear, that inflammation does not accompany only infectious diseases but also others, causing cell, tissue or organ injury and serves primarily defensively (Table 1). An exaggerated, chronic long lasting or non-adequately regulated inflammatory response could be the cause of adverse reactions and could lead to pathology (Bucova, 2002b). Inflammation plays an important role also in the etiology of ischemic heart disease (IHD), myocardial infarction (MI), angina pectoris (AP) and hypertension, however, its mechanism in various stages of pathological process is not well understood (Bucova et al., 2008a; Itoh et al., 2007; Kuka et al., 2010; Li, 2005; Pickering et al., 2007, Ross 1999). If the cause of IHD is atherosclerosis or other, it is accompanied by inflammation. Various types of inflammatory cells, cytokines, chemokines and other soluble factors were confirmed to be involved in this process. (Armstrong et al 2006; Aukrust et al., 2001; Brunetti et al., 2006; Bucova et al., 2008a; Ferencik et al., 2007).