Scientific background

scientific background


Within hours after successful reperfusion, a well-orchestrated healing mechanism is initiated. White blood cells, fibroblasts, dendritic cells and other progenitor cells from peripheral organs and blood are mobilized upon the release of signals related tissue injury. A first rapid mobilization of neutrophils, chemo- and cytokines into the heart paves the way for secondary migration waves of other leukocyte subtypes, such macrophages, lymphocytes and dendritic cells. Eventually, cell debris within the infarcted area is removed and replaced by proteins secreted into the extracellular environment (extracellular matrix). This is the stage in which a provisional matrix is formed that regulates scar formation and vessel growth. Fibronectin-EDA is a major component of the provisional matrix responsible for a series of adverse events in both the infarcted as well as unaffected remote myocardium.

Fibronectin-EDA is a large adhesive glycoprotein that is generated by alternative splicing from a single gene. It interacts with other extracellular matrix proteins and cellular ligands and receptors, such as glycosaminoglycans, collagen, fibrin, integrins and Toll-like receptors. Fibronectin-EDA is prominently expressed during embryogenesis and remains absent hereafter in healthy tissue. However, its expression becomes evident after injury, such as AMI. Pre-clinical translational studies are pending to explore the full potential of EnCare Biotech products.