Cardiac disease causes morbidity and mortality as frequently as cancer, yet predicting arrhythmia and understanding the underlying genetic mechanisms remains a major challenge. Our goal is to bridge this gap using patient-specific stem cell technologies.
Disease Modelling and Gene Editing
We derive human induced pluripotent stem cells (hiPSCs) from patients to capture their specific genetic background. We use the CRISPR-Cas technology for correcting the gene mutations.
These cells are differentiated into contracting cardiomyocytes and other cells of the heart.
By comparing mutated and corrected hiPSC-cardiac cells, we can discover molecular mechanisms underlying inherited cardiac arrhythmia and other pathological phenotypes.
We also use gene editing to generate hiPSC reporter lines.
Drug Testing
We use hiPSC-derived cardiac cells to
Develop drug-screening platforms to identify molecules that can rescue disease phenotypes.
Assess safety pharmacology, identifying compounds with potential cardiotoxic effects before they reach clinical trials.
Test gene editing tools able to reverse pathological phenotypes
3D Cardiac Microtissues and kidney organoids
The heart is not just cardiomyocytes; it is a complex tissue involving endothelial cells, fibroblasts, and connective tissue. To accurately reproduce this environment, we have developed 3D-cardiac microtissue constructs, that we call “Mini-Heart”. By combining cardiomyocytes with non-myocyte cells, we mimic the multicellular organization and dynamic function of the native heart. These advanced models are crucial for more reliable disease modelling and drug screening results.
Finally, renal-cardiac crosstalk plays a key role in health and disease. We have combined our cardiac microtissues with kidney organoids in the lab to support the capture of inter-organ communication.