• Marina CAMPIONE
    Title: C.N.R. Senior Scientist
    Telephone: 049 827-6031
    E-mail: campione@bio.unipd.it
    Group Website: [link]

Current position:

2001-present: Research Scientist, Neuroscience Institute, National Research Council (CNR), Padua. 



2000-2001: Telethon fellow, Dept. of Biomedical Sciences, University of Padua.

1998-2000: Postdoctoral Fellow, Dept. of Experimental and Molecular Cardiology, Academic Medical Center, Amsterdam, The Netherlands.

1995–1998: Postdoctoral Fellow, Institute for Genetics, Karlsruhe, Germany.

1995: PhD degree in Molecular and Cellular Biology and Pathology, University of Padua. 


Dr. Campione studies the molecular basis driving cardiac development and the impact of developmental processes on the functional properties of the adult heart. Ongoing research activity:

1)Understanding cardiac laterality: the role of the homeobox gene Pitx2. 

By employing constitutive and myocardial specific Pitx2 knock out (ko) mice, we have shown that Pitx2 determines the morphological and molecular identity of the left sino-atrial region during development. Pitx2 ko mice have normal looping directionality but present severe ventricular remodeling defects, associated to impaired cardiomyocyte cytoarchitecture and maturation. We are presently characterizing the cellular basis for Pitx2 contribution to atrial septation and to ventricular remodeling. 

Reduced dosage of the Pitx2 gene has been shown to increase susceptibility to atrial fibrillation in humans and in mice, thus linking laterality to adult heart function. We are additionally exploiting Pitx2 mutant mice to dissect the regional contributions of Pitx2 to arrhythmogenesis.

2)The role of mechanosensing genes in cardiac development and in modulation of adult heart functionality.

Cardiomyocytes, the functional units of the heart, can sense and transduce environmental cues such as mechanical stress and hemodynamics. Mutations in myofibrillar and associated genes can result in congenital heart disease (CHD), thus suggesting that compromise of early function can also affect heart development. We are currently characterizing a novel transgenic mouse model overexpressing a mechanosensor gene which is mutated in CHD patients and is upregulated in adult cardiomyopathy.

1. Ulmer B, Tingler M, Kurz S, Maerker M, Andre P, Mönch D, Campione M, Deißler K, Lewandoski M, Thumberger T, Schweickert A, Fainsod A, Steinbeißer H, Blum M. (2017). A novel role of the organizer gene Goosecoid as an inhibitor of Wnt/PCP-mediated convergent extension in Xenopus and mouse. Sci Rep.;7:43010. 

2. Campione M and Franco D. Current Perspectives in Cardiac Laterality (2016).  J. Cardiovasc. Dev. Dis. 2016, 3(4), 34.

3. Zaglia T, Pianca N, Borile G, Da Broi F, Richter C, Campione M, Lehnart SE, Luther S, Corrado D, Miquerol L, Mongillo M. (2015). Optogenetic determination of the myocardial requirements for extrasystoles by cell type-specific targeting of ChannelRhodopsin-2. Proc Natl Acad Sci U S A.;112(32):E4495-504. 

4. Ammirabile G, Tessari A, Pignataro V, Szumska D, Sardo FS, Benes J Jr, Balistreri M, Bhattacharya S, Sedmera D, Campione M.(2012). Pitx2 confers left morphological, molecular, and functional identity to the sinus venosus myocardium. Cardiovasc Res. 93,291-230.  

5. Tessari A, Pietrobon M, Notte A, Cifelli G, Gage PJ , Schneider MD, Lembo G, Campione M.(2008). Myocardial Pitx2 differentially regulates the left atrial identity and ventricular asymmetric remodelling programs. Circ. Res 102,813-822.