Myocardial stabilin-1-positive macrophages in patients with fatal myocardial infarction

Cardiac remodeling following myocardial infarction leads to impaired ventricular function and heart failure which remain a major cause of mortality and morbidity. The need to extend our knowledge about what factors lead to different outcomes of myocardial infarction has led to a research of immuno-inflammatory pathways and molecular activities as the basis of post-infarction remodeling. Recently, macrophages, cells of the immune system, became a subject of scientific interest both under normal and pathological conditions. There are two subpopulations of macrophages: inflammatory M1 macrophages and M2 macrophages, which perform adaptive, regenerative, and anti-inflammatory function. One of the M2 macrophage biomarkers is scavenger receptor stabilin-1. M2 macrophages, expressing stabilin-1, mediate degradation of acetylated low-density lipoproteins and glycoprotein SPARC (secreted protein acidic and rich in cysteine), a universal regulator of wound healing, angiogenesis and tissue remodeling. The aim of this study was to show the presence/absence of myocardial stabilin-1-positive macrophages in patients with fatal myocardial infarction by means of immunohistochemistry. Data confirming the presence of stabilin-1-positive macrophages M2 allow for continuing further studies to identify the molecular profile and function of these cells in the development of adverse cardiac remodeling.