Abstract
Fibrosis induced by prolonged inflammation is a major pathophysiological feature of adverse left ventricular remodeling after myocardial infarction and pathological cardiac hypertrophy. Recent reports strongly suggest that the interaction between leukocytes, non-myocytes (mainly cardiac fibroblasts) and cardiomyocytes, possibly mediated by cytokine signaling, plays an important role in controlling the inflammatory reaction after cardiac injury. Therefore, controlling cytokine secretion from resident cardiomyocytes is one plausible strategy for preventing tissue damage.