CCL2 and endothelial dysfunction: This increases the release of proinflammatory cytokines, such as tumour necrosis factor-α, interleukin-6, monocyte chemoattractant protein-1, and other factors, and coagulation-promoting factors and adhesion molecules, which are also associated with myocardial oxidative stress and endothelial dysfunction [33–35], leading to a vicious cycle.