Abstract
Background and Aims : Coronary artery disease (CAD) is a globally leading cause of death and brought about by atherosclerosis prompted by a multifactorial interplay of genetic and lifestyle factors. Mechanisms resulting in CAD can be grouped into different pathways. However, characterization and regulation of these tissue specific functional networks is far from being complete. We aimed to experimentally study the regulatory capacities of promising targets and identify new therapeutical concepts to decrease CAD risk.
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