The contribution of the cardiomyocyte to tissue inflammation in cardiomyopathies.

Cardiac injury triggers an acute immune response that drives tissue healing and remodeling via the activation of compensatory mechanisms. Over time, remodeling and inflammation become chronic and have adverse effects that lead to a depression of cardiac function and eventual heart failure. Cardiac inflammation is characterized by dynamic spatial and temporal crosstalk between the resident cells of the heart and recruitment of circulating leukocytes. Until recently, the cardiomyocyte has not been accepted as a direct contributor to cardiac inflammation. It has now emerged as a key initiator of the acute immune response via its ability to produce cytokines and may also synchronize leukocyte recruitment post-injury. This review will focus on the role of the cardiomyocyte in the acute immune response to ischemic and non-ischemic injury and the mechanisms by which it may influence the course of cardiac remodeling and failure.