Complexity is not necessarily expected from monogenic diseases but for many cardiovascular diseases (CVD), simple genotype-phenotype relationship may be far from reality. As millions of people... Show moreComplexity is not necessarily expected from monogenic diseases but for many cardiovascular diseases (CVD), simple genotype-phenotype relationship may be far from reality. As millions of people globally die of CVD, it is important to find models to study CVD that recapitulate the conditions as manifest in humans, most importantly for these cases of unexpected complexity. For these, simple gene mutation or deletion in mice has often failed. Combining human induced pluripotent stem cell (hiPSC) with genetic editing technologies is providing new opportunities to bridge the gap, with many hPSC-CM models now showing promising results for testing drugs, discovering molecular pathways associated with disease and other types of (gene) therapies. The work in this thesis contributes to this area of research. Show less
