Role of Adenosine and Purinergic Receptors in Myocardial Infarction: Focus on Different Signal Transduction Pathways

Myocardial infarction (MI) is a dramatic event often caused by atherosclerotic plaque erosion or rupture and subsequent thrombotic occlusion of a coronary vessel. The low supply of oxygen and nutrients in the infarcted area may result in cardiomyocytes necrosis, replacement of intact myocardium with non-contractile fibrous tissue and left ventricular (LV) function impairment if blood flow is not quickly restored. In this review, we summarized the possible correlation between adenosine system, purinergic system and Wnt/beta-catenin pathway and their role in the pathogenesis of cardiac damage following MI. In this context, several pathways are involved and, in particular, the adenosine receptors system shows different interactions between its members and purinergic receptors: their modulation might be effective not only for a normal functional recovery but also for the treatment of heart diseases, thus avoiding fibrosis, reducing infarcted area and limiting scaring. Similarly, it has been shown that Wnt/beta catenin pathway is activated following myocardial injury and its unbalanced activation might promote cardiac fibrosis and, consequently, LV systolic function impairment. In this regard, the therapeutic benefits of Wnt inhibitors use were highlighted, thus demonstrating that Wnt/beta-catenin pathway might be considered as a therapeutic target to prevent adverse LV remodeling and heart failure following MI.

Automated summary

Myocardial infarction is often caused by atherosclerotic plaque erosion or rupture leading to thrombotic occlusion of a coronary vessel. The inadequate oxygen and nutrient supply in the infarcted area can result in cardiomyocyte necrosis and left ventricular function impairment. The adenosine system, purinergic system, and Wnt/beta-catenin pathway may play crucial roles in the pathogenesis of cardiac damage following MI, with potential therapeutic implications in preventing adverse LV remodeling and heart failure.