The pronounced inability of adult human/mammalian heart to regenerate causes millions of deaths following cardiac insult, particularly in the longer term. The extent and persistence of associated inflammation has been generally linked with adverse cardiac outcomes, including fibrosis, hypertrophy, and dysfunction. However, characteristics of the inflammatory response e.g. the maturity of resident macrophages and/or the activation status of infiltrating cells may differentially influence cardiac fibroblasts and, most importantly, cardiomyocytes, thus affecting cardiac regeneration, hypertrophy, fibrosis and dysfunction. Unraveling crucial parameters of such interactions in appropriate biological systems should confer decisive intervention potential in a serious health problem. In the past years we have studied in detail cellular and molecular players regulating pivotal events initiating or sustaining the progress to heart failure (HF) in mice and zebrafish and we propose here to combine the systems to globally study these interactions.
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