Defensin-chemokine heteromeric complexes derived from heterocellular activation—a possible target to inhibit CCL5 in cardiovascular settings
Ischemic heart disease is one of the leading causes of death all over the world even after several medical technologies such as revascularization therapy including catheter intervention and surgery, and drug treatment have been developed. Among them, acute myocardial infarction (AMI) is caused by sudden occlusion of coronary arteries induced by atherosclerotic plaque rapture or vasospasm. Consequently, cardiomyocytes downstream of the culprit site are exposed to hypoxia and eventually die, which induces acute pump failure, fatal arrhythmia, acute valvular dysfunction, cardiac rupture and so on. Even after surviving this acute period, pathological cardiac remodeling changes left ventricular size, mass and function, and leads to several chronic complications such as heart failure and ventricular arrhythmia, which finally increases the mortality. Therefore, development of new treatment strategy for this life-threatening disease is required.