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Our Research

Experimental Approaches:

Our research involves:

  • Human and mouse primary cells

  • iPS derived cardiomyocytes and cardiac fibroblasts

  • Advanced mouse models for gene knockout and lineage tracing

  • Single cell and bulk multiomics (RNA-seq, ATAC-seq and ChIP-seq) combined with advanced bioinformatics

  • Genome editing using CRISPR-Cas9

  • High resolution microscopy imaging

  • Standard cellular and molecular biology techniques

Research lines:

Transcriptional and Epigenetic Regulation of Cardiac Development

Approximately 1 in 100 children is affected by congenital heart disease, but the causative factors for these defects remain largely elusive. Often, they are linked to alterations in key molecular pathways. To better comprehend the cause of these diseases, we are studying the transcriptional and epigenetic mechanisms involved in controlling correct cardiac morphogenesis. Using sophisticated transgenic mouse models, we are investigating whether alterations in these mechanisms are responsible for cardiac morphogenic defects. We have identified that the histone methyltransferase Dot1L is essential for proper expression of key cardiac transcription factors during embryonic development and is furthermore required for postnatal cardiomyocyte cell cycle withdrawal.

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Exploring Micropeptides for Cardiac Regeneration

Micropeptides, are a relatively new class of proteins that despite their small size can play major roles in cellular functions. Utilizing cutting-edge translatomic and proteomic approaches we are identifying micropeptides that are conserved across species and modulated during cardiomyocyte maturation. Furthermore, we are defining their cellular functions and exploring their potential to induce proliferation of cell cycle withdrawn cardiomyocytes or enhance maturation of iPS cell-derived cardiomyocytes, and ultimately develop new gene  and cell therapy approaches. 


Cardiac Fibrosis

Cardiac fibrosis, is characterized by the excessive deposition of extracellular matrix by activated fibroblasts, and is considered a hallmark of heart failure, regardless of the etiology. Prolonged cardiac fibrosis results in cardiac remodeling which leads to the stiffening of the heart and eventual failure. Developing strategies to control the extent of fibrotic remodeling is of utmost importance, as efficient anti-fibrotic treatments remain an unmet clinical need. In this context, our ongoing projects focus on:

1.    Identifying the origin of activated fibroblasts.

2.    Studying the heterogeneity of fibroblasts

3.    Identifying molecular targets, including regulatory elements and transcription factors, that regulate fibroblast activation and that

       can be manipulated to control the timing and extent of fibrotic responses.

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