Chemokines and inflammation in heart disease: adaptive or maladaptive?

Heart disease is not only the leading cause of death, disability, and healthcare expense in the US, but also the leading cause of death worldwide. Therefore, treatments to lessen ischemia-related cardiac damage could affect a broad swath of the population and have significant health and fiscal impacts. Cardiac dysfunction has been associated with elevated circulating chemokine levels, both in animals and humans. Most studies in this area have focused on chemokine expression as a prominent feature of the post-infarction inflammatory response. Such studies have investigated the role of chemokines in inflammatory leukocyte recruitment. Other work on this topic has focused on stem-cell therapy or factors e.g. chemokines mobilizing bone marrow progenitor cells as possible avenues for improving contractile dysfunction. Findings from numerous preclinical studies and several initial clinical trials support the feasibility of promoting the recruitment of bone marrow-derived cells to the infarcted heart and increased homing following injury, supporting the notion that cell therapy might have therapeutic potential. They have not, however, addressed the possibility of an autocrine/paracrine effect wherein the chemokine receptors, present on the cardiac myocyte surface, modulate functional responses to stress in which can be adaptive or maladaptive in nature.