Fig. 4

Schema of inflammatory circuits induced by 2-AG in cardiac diseases. Concentrations of 2-AG correlate with the severity of coronary artery disease. Upon 2-AG treatment, immune signaling cascades lead to an enhanced expression of immune-modulatory cytokines like TNFα via JAK, STAT3 and NFκB. Hypothetically, enhanced levels of released cytokines have a systemic effect but also local effects on resident cells of the cardiac tissue, like macrophages, cardiomyocytes, fibroblasts and endothelial cells. With disease progression this inflammatory circuit is increasingly active and leads to the production of CRFs in cardiac tissue.