Stefano Schiaffino - Short Biography#


I am Professor Emeritus of General Pathology, University of Padova. I obtained the degree in Medicine in 1963 from the University of Modena and I was Professor at the Department of Biomedical Sciences (formerly Institute of General Pathology) in the School of Medicine of the University of Padova from 1965 to 2010. I was visiting scientist at INSERM U127 Hôpital Lariboisière in Paris in 1986-1987 and Director of the CNR (Italian National Research Council) Centre of Muscle Biology and Physiopathology from 1988 to 2002. About 20 years ago I founded, with some colleagues of the University of Padova, a private research center, the Venetian Institute of Molecular Medicine (VIMM), where I am presently working.

During the first part of my career I have been mostly interested in defining the heterogeneity of muscle cells in skeletal and cardiac muscle using first electron microscopy and then immunocytochemistry. For many years my work has focused on the characterization of myosin heavy chain isoforms in mammalian skeletal muscle. We prepared a battery of specific anti-myosin monoclonal antibodies that are widely used in many labs. An important result of these studies has been the discovery in skeletal muscle of a novel fast-type myosin, called type 2X, and a corresponding muscle fibre type, distinct from the traditional fast 2A and 2B fibres. We also found that different myosins are present in atrial and ventricular myocardium and in the heart conduction tissue, thus revealing the existence of molecular markers specific for different cardiac cell populations.

During the last 20 year I was mostly interested in cell signalling in adult skeletal muscle, focusing on the mechanisms that control fibre type specification and atrophy/hypertrophy changes. Using an in vivo transfection approach based on intramuscular injection of plasmid DNA, we generated selective perturbations of different signalling pathways with constitutively active or dominant negative constructs and examined the effect of these perturbations in transfected fibres. A major aim has been the identification of the pathways that mediate the effect of nerve activity on the muscle phenotype. We found that the Ras-ERK and calcineurin-NFAT pathways control activity-dependent fibre type specification, while the Akt-mTOR and Akt-FoxO pathways control the atrophy/hypertrophy processes. Our most recent studies showed that FoxO transcription factors control the two main pathways of protein degradation in muscle cells, the proteasomal and autophagic-lysosomal pathways. The dissection of the mechanisms controlling the muscle phenotype should provide a better understanding of clinically relevant issues, including the beneficial effect of physical exercise and the cause of muscle atrophy and loss of force during aging.

A complete list of my publications can be found here: https://scholar.google.it/citations?user=x8Y43UYAAAAJ&hl=it&oi=ao

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