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What we do

During heart development, the cardiac progenitor cells (CPCs) differentiate into the functional cells of the heart, including atrial, ventricular and nodal cells. The differentiation toward specific cardiac lineages is controlled by complex regulatory networks involving multiple signaling pathways, transcription factors and chromatin regulators. Some mutations and/or environmental agents perturb these cardiac regulatory networks to alter the differentiation of CPCs toward specific lineages, giving rise to developmental abnormalities of the heart. These abnormalities are commonly known as congenital heart defects (CHD). The goal of our laboratory is to identify the key players of these networks and how they incorporate into the regulatory circuitries that guide specific cell fate decisions. This knowledge is essential to understand the etiology of CHD and may help to isolate potential therapeutic targets and, provide new diagnostic or outcome-prediction tools.

Why do we study this?

Nearly 1% of babies are born with a Congenital Heart Defect (CHD), the most common developmental defect and one of the leading cause of death in children. Children and adults with CHD face a life-long risk of health problems, and current therapies are limited to corrective surgery and heart transplant. We believe that by investigating the roots of the heart developmental defect we will be able to provide new tools to treat CHD.

Our approach

The main models of study in our lab are the human embryonic stem cells (hESCs) and induced Pluripotent Stem Cells (iPSCs) from patients carrying CHD. We aim to recapitulate the early stages of cardiac development by applying both directed differentiation strategies together with 3D differentiation approaches. We apply a wide-range of techniques to obtain a comprehensive panel of the transcriptome and the epigenome of the cells during the acquisition of specific cardiac cell fates. We are also introducing mouse models in the lab to investigate the process of cardiac lineage acquisition and heart regeneration in vivo.