M
Matteo Dal Ferro
Researcher at University of Trieste
Publications - 65
Citations - 2231
Matteo Dal Ferro is an academic researcher from University of Trieste. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 15, co-authored 36 publications receiving 1562 citations. Previous affiliations of Matteo Dal Ferro include International Centre for Genetic Engineering and Biotechnology.
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Journal ArticleDOI
Functional screening identifies miRNAs inducing cardiac regeneration
Ana Eulalio,Miguel Mano,Matteo Dal Ferro,Matteo Dal Ferro,Lorena Zentilin,Gianfranco Sinagra,Serena Zacchigna,Mauro Giacca +7 more
TL;DR: It is shown that the exogenous administration of selected microRNAs (miRNAs) markedly stimulates cardiomyocyte proliferation and promotes cardiac repair and the miRNAs identified hold great promise for the treatment of cardiac pathologies consequent to cardiomeocyte loss.
Journal ArticleDOI
Truncating FLNC Mutations Are Associated With High-Risk Dilated and Arrhythmogenic Cardiomyopathies
Martin Ortiz-Genga,Sofía Cuenca,Matteo Dal Ferro,Esther Zorio,Ricardo Salgado-Aranda,Vicente Climent,Laura Padron-Barthe,Iria Duro-Aguado,Juan Jiménez-Jáimez,Víctor M. Hidalgo-Olivares,Enrique García-Campo,Chiara Lanzillo,M. Paz Suárez-Mier,Hagith Yonath,Sonia Marcos-Alonso,Juan Pablo Ochoa,José L. Santomé,Diego García-Giustiniani,Jorge Rodriguez-Garrido,Fernando Dominguez,Marco Merlo,Julián Palomino,Maria Luisa Peña,Juan Pablo Trujillo,Alicia Martín-Vila,Davide Stolfo,Pilar Molina,Enrique Lara-Pezzi,Francisco E. Calvo-Iglesias,Eyal Nof,Leonardo Calò,Roberto Barriales-Villa,Juan Ramón Gimeno-Blanes,Michael Arad,Pablo García-Pavía,Lorenzo Monserrat +35 more
TL;DR: In this article, the authors demonstrate the association between truncating mutations in the Filamin C (FLNC) gene and the development of high-risk dilated and arrhythmogenic cardiomyopathies.
Journal ArticleDOI
Genetic Risk of Arrhythmic Phenotypes in Patients With Dilated Cardiomyopathy
Marta Gigli,Marco Merlo,Sharon L. Graw,Giulia Barbati,Teisha J. Rowland,Dobromir Slavov,Davide Stolfo,Mary E. Haywood,Matteo Dal Ferro,Alessandro Altinier,Federica Ramani,Francesca Brun,Andrea Cocciolo,Ilaria Puggia,Gaetano Morea,William J. McKenna,Francisco G. La Rosa,Matthew R.G. Taylor,Matthew R.G. Taylor,Gianfranco Sinagra,Luisa Mestroni,Luisa Mestroni +21 more
TL;DR: Desmosomal and LMNA gene variants identify the subset of DCM patients who are at greatest risk for SCD and life-threatening ventricular arrhythmias, regardless of the left ventricular ejection fraction.
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Regional Variation in RBM20 Causes a Highly Penetrant Arrhythmogenic Cardiomyopathy
Victoria N. Parikh,Colleen Caleshu,Chloe M. Reuter,Laura C. Lazzeroni,Jodie Ingles,John Garcia,Kristen McCaleb,Tolulope Adesiyun,Farbod Sedaghat-Hamedani,Saurabh Kumar,Sharon L. Graw,Marta Gigli,Davide Stolfo,Matteo Dal Ferro,Alexander Y Ing,Robert L. Nussbaum,Birgit Funke,Matthew T. Wheeler,Ray E. Hershberger,Stuart A. Cook,Lars M. Steinmetz,Neal K. Lakdawala,Matthew R.G. Taylor,Luisa Mestroni,Marco Merlo,Gianfranco Sinagra,Christopher Semsarian,Benjamin Meder,Benjamin Meder,Daniel P. Judge,Euan A. Ashley +30 more
TL;DR: These findings underline the importance of arrhythmia surveillance and family screening in this disease and represent the first step in defining the genetic architecture of RBM20 disease causality on a population level.
Journal ArticleDOI
The K219T-Lamin mutation induces conduction defects through epigenetic inhibition of SCN5A in human cardiac laminopathy.
Nicolò Salvarani,Silvia Crasto,Michele Miragoli,Michele Miragoli,Alessandro Bertero,Marianna Paulis,Paolo Kunderfranco,Simone Serio,Alberto Forni,Carla Lucarelli,Matteo Dal Ferro,Veronica Larcher,Gianfranco Sinagra,Paolo Vezzoni,Charles E. Murry,Giuseppe Faggian,Gianluigi Condorelli,Gianluigi Condorelli,Elisa Di Pasquale +18 more
TL;DR: It is shown that patient-specific iPSC-derived CMs carrying the K219T LMNA mutation have downregulated Nav1.5 channels due to dynamic cooperation of Lamin A/C and Polycomb repressor complex 2 at the SCN5A promoter.