In his HCEMM project (entitled as “Cardiac inflammation: a new therapeutic target in myocardial dysfunctions”), his junior group aims to define the relationship between heart failure and cardiomyopathy and non-alcoholic steatohepatitis (NASH). Accumulating evidence suggests that pro-inflammatory pathways and systemic inflammation (seen e.g. is NASH) play an essential role in the development of myocardial dysfunction and heart failure. Recently new mechanisms and molecular components have been identified being involved in triggering proinflammatory milieu, however their contribution to cardiac derangements (fibrosis, myocardial dysfunction, microvascular dysfunction) remains elusive. Therefore, his group intends to i) setup an animal model of NASH that associates with myocardial dysfunction, and to ii), investigate whether the newly identified mechanisms, co-morbidities (e.g. steatohepatitis), and pro-inflammatory mediators play a role in failing hearts in the NASH animal models iii) to characterize inflammatory mechanisms in human end-stage heart failure samples and to propose reverse translational animal models of chronic heart failure for drug testing. By using newly established models, they will determine the effect of inflammation on myocardial function, morphology, histology and molecular alterations (inflammation-, hypertrophy-, apoptosis-, and autophagy-related pathways). Based on these results the cardiac effect of pharmacologic modulation of novel inflammatory pathways will be also tested in the newly established animal models.