Fig. 1

a Paradigms dealing with mechanisms of cardiac remodeling after myocardial infarction. In the early phase of injury, ventricular remodeling is an effect of infarct expansion; in late phase it involves reactive myocyte hypertrophy, interstitial fibrosis and left ventricular dilatation. Changes of the extracellular collagen matrix in infarct heart play an important role in cardiac remodeling A huge number of endogenous factors affect the extracellular collagen matrix in different ways, causing degradation or synthesis of its components. b Cardiomyocyte necrosis triggers an activation of innate immune system and a cascade of inflammatory pathways. In response to ischemic injury monocytes are recruited from the bone marrow and spleen to the heart and become monocyte-derived macrophages. Macrophages produce pro- and anti-inflammatory factors, promote resorption of cellular debris, regulation of granulation tissue formation and neoangiogenesis. The search of therapeutic target, which is able to prevent, limit or reverse adverse cardiac remodelingg is one of the most important and complicated tasks of modern cardiology