Which are the disease mechanisms responsible for inherited cardiomyopathies associated to sudden death?
How to treat such disorders?

Our research aims at identifying the molecular mechanisms underlying familial cardiomyopathies, such as ACM and FHC, both representing leading causes of sudden death in the young population. Our purpose is to recognize novel mechanism-driven therapeutic strategies to counteract disease onset and progression. To reach our goals, we benefit from collaborations with other groups within the VIMM, the clinical Department of Cardiology and other national and international laboratories. In our research, we analyse heart tissue using 2-photon, fluorescence and electron microscopy, biochemical and molecular methods, as well as in vitro model systems to understand the molecular mechanisms of cardiac diseases.

Arrhythmogenic Cardiomyopathy (ACM) is a genetically determined cardiac disease, mainly caused by mutations in genes encoding for desmosomal proteins. ACM represents the most frequent cause of sudden death in young athletes. Hearts of ACM patients show cardiomyocyte (CM) death, inflammation and fibro-fatty tissue replacement. The clinical phenotype is characterized by ventricular arrhythmias often triggered by physical stress, such as exercise, which has also been shown to accelerate ACM progression. The pathogenesis of myocardial fibro-fatty remodeling is not yet understood, also because the current experimental models only partially recapitulate the human ACM phenotype.

Familial Hypertrophic Cardiomyopathy (FHC) is the most common genetic disease of the heart, and is mainly caused by mutations in genes encoding for proteins of the sarcomere, the contractile unit of cardiac cells. The disease causes enlargement in the heart size, and manifests with symptoms ranging from weakness and exercise intolerance to severe heart failure and arrhythmias, generally worsening with age. To date, the mechanisms causing FHC are largely undetermined and current therapies are unsuccessful in preventing the progressive cardiac dysfunction. Recently, it has been suggested that the presence in cardiac cells of the incorrect protein, encoded by the mutated gene, overloads the main systems used by cells to remove old and damaged proteins, that is to say, the Ubiquitin Proteasome System (UPS) and the autophagy/lysosome system (ALS), essential in the control of cardiac protein homeostasis.


  • PhD: Dept. of Pathological Anatomy, University of Padova, Italy (2007)
  • Postdoc: Dept. of Biomedical Sciences, University of Padova, Italy (2007-2011)
  • Research Fellowship: Venetian Institute of Molecular Medicine, Padova, Italy (2011-2013)
  • Telethon Junior Researcher: Venetian Institute of Molecular Medicine, Padova, Italy (2013-2016)
  • Assistant Professor: Department of Cardiac, Thoracic and Vascular Sciences, University of Padova, Italy (since 2017)
  • Junior Principal Investigator: Venetian Institute of Molecular Medicine, Padova, Italy (since 2017)

Selected Awards

  • 2016 – Best poster presentation. FCVB (ESC), Florence
  • 2012 – Young Investigator Award, Heart Failure (ISHR), Belgrade
  • 2012 – Best poster presentation. FCVB (ESC), London

Current funding