## 4 Discussion
Although the overexpression of iNOS has been associated with septic shock, some autoimmune diseases, and even malignancies, it also has beneficial effects and is necessary for normal cellular function [49]. Interestingly, some studies suggest that the concomitant presence or absence of oxidative stress is important in maintaining the balance between the beneficial and detrimental effects of iNOS [50]. However, in the present study, no alterations in oxidative stress biomarkers were detected in any of the dietary protocols. In transgenic mice overexpressing human endothelin-1 (ET-1), the knockout of iNOS resulted in impaired endothelium-dependent vasodilation [51]. Although the increased expression of iNOS was thought to contribute to the occurrence of cardiogenic shock in individuals with myocardial infarction, iNOS inhibitors did not show beneficial effects in this group of individuals. Moreover, NO might actually be important for better recovery after cardiac events [52]. Overall, vitamin E, selenium, and n-3 PUFAs are important in maintaining the endothelial balance, and their supplementation may contribute to better endothelial function in CCS patients [11; 37; 38]. An important result of the present study is the reduced levels of IL-17A and TGF-1 \(\beta\) after the consumption of Nutri4 eggs. IL-17A is one of the cytokines involved in the defense against a variety of microbial pathogens, as well as tissue inflammation. Its role in autoimmune diseases (for example, rheumatoid arthritis, inflammatory bowel diseases, asthma, psoriasis, and multiple sclerosis) is well known, but its influence on the pathophysiological mechanisms involved in the development of endothelial dysfunction and consequent atherosclerosis has not been fully elucidated [53]. IL-17A induces the release of chemokines that stimulate the recruitment of neutrophils and monocytes to the atherosclerotic lesion area. IL-17A also stimulates macrophages to produce other inflammatory cytokines (IL-6, TNF-\(\alpha\), IL-1\(\beta\)) and promotes a pro-atherogenic phenotype [54]. Some studies suggest that IL-17A has a proinflammatory effect, while others suggest that it is an anti-inflammatory cytokine that depends on other cytokines in its environment [55; 56]. The expression of IL-17A has been associated with increased inflammation and plaque susceptibility in human atherosclerotic lesions [52]. Interestingly, statins, which are lipid-lowering agents (also taken by our patients), can downregulate inflammatory responses and stabilize atherosclerosis plaques, as well as inhibit the proinflammatory, thrombotic, and aggregation effects of IL-17 on vessels [57]. Importantly, in patients with rheumatoid arthritis, vitamin E reduces Th17 differentiation and inhibits IL-17-activated osteoclast formation, and another study suggests that n-3 PUFAs decrease IL-17A levels in vitro in stem cells derived from the adipose tissue of subjects with obesity [58; 59], which may explain the decrease in IL-17A in CCS patients who consumed enriched eggs in this study (and had increased plasma vitamin E concentrations). In addition to IL-17A, the consumption of nutrient-enriched eggs resulted in lower levels of TGF-\(\beta\)1, an important cytokine in cell-to-cell signaling [60]. Dysregulated TGF-\(\beta\)1 signaling can cause arteriovenous malformations, aneurysms, atherosclerosis, cardiac fibrosis, and valvular heart disease in humans. Endothelial TGF-\(\beta\)1 plays an important role in signal transduction and atherosclerosis-associated vascular inflammation [61]. The effect of TGF-\(\beta\) on atherosclerosis depends on the balance between pro- and anti-atherogenic signaling pathways [62]. Coronary artery atherosclerotic plaques have elevated TGF-\(1\beta\) levels, and higher levels are also associated with stable plaques in chronic coronary syndrome [63]. In a mouse model with hyperlipidemia, after the inhibition of endothelial TGF-\(\beta\) signaling, there was a decrease in the inflammation of the vessel wall and further progression of atherosclerotic changes [64].