Significance
Heart diseases are the leading cause of death worldwide. Oxidative stress is a common unwanted outcome that especially occurs due to the reperfusion following heart attack or heart surgery. Standard methods of in vivo analysis do not allow dissecting various intermingled parameters, while regular 2D cell culture approaches often fail to provide a biomimetic environment for the physiologically relevant cellular phenotypes. In this research, a systematic genome-wide transcriptome profiling was performed on myocardial cells in a biomimetic 3D hydrogel-based synthetic model tissue, for identifying possible target genes and pathways as protecting regulators against oxidative stress. Identification of such pathways would be very valuable for new strategies during heart disease treatment by reducing the cellular damage due to reperfusion injury.
Statement of significance
Heart diseases are the leading cause of death worldwide. Oxidative stress is a common unwanted outcome that especially occurs due to the reperfusion following heart attack or heart surgery. Standard methods of in vivo analysis do not allow dissecting various intermingled parameters, while regular 2D cell culture approaches often fail to provide a biomimetic environment for the physiologically relevant cellular phenotypes. In this research, a systematic genome-wide transcriptome profiling was performed on myocardial cells in a biomimetic 3D hydrogel-based synthetic model tissue, for identifying possible target genes and pathways as protecting regulators against oxidative stress. Identification of such pathways would be very valuable for new strategies during heart disease treatment by reducing the cellular damage due to reperfusion injury.