- Vivi Padova
- Il Bo
High School Diploma Liceo Classico “Paolo Diacono”, Cividale del Friuli (Italy) 1971
M.D. Degree: University of Padova (Italy), cum laude 1978
1979 – 1987: Assistant Professor, University of Padova Medical School
1988 – 1999: Associate Professor, University of Padova Medical School
2000 – present: Full Professor, University of Padova Medical School
2001 – 2004: Deputy Dean of the Medical Faculty, University of Padova
2003 – 2009: Chairman, Department of Biomedical Sciences, University of Padova
2012 – present: Director, Postgraduate School of Clinical Pathology, University of Padova
2012 – present: Coordinator, Ph.D. Program in Cell Biology, University of Padova
Paolo Bernardi began his studies on mitochondrial physiology and ion transport under the guidance of Giovanni Felice Azzone, one of the founding Fathers of Bioenergetics. His education in Cellular and Molecular Biology was completed with a long-term stay at the Whitehead Institute for Biomedical Research - Massachusetts Institute of Technology, where he worked under the supervision of Harvey F. Lodish.
He pioneered the field of mitochondrial channels and their role in cellular pathophysiology. In particular, he focused on the permeability transition pore (PTP), a high conductance channel that is increasingly recognized as a key player in cell death. During the early 1990s he defined key points of regulation of the PTP in isolated mitochondria (membrane potential, matrix pH, Me2+-binding sites, specific redox-sensitive sites).
He then developed tools to reliably monitor mitochondrial function in situ, and addressed mechanistic questions on the PTP as a target in degenerative diseases and cancer.
His studies have been extended to in vivo models, and led to the demonstration that early mitochondrial adaptation plays a key role in hepatocarcinogenesis [Klöhn et al. (2003) Proc Natl Acad Sci USA 100, 10014-10019] and in onset of the Warburg effect [Sciacovelli et al. (2013) Cell Metab 17, 988-999]; and that mitochondrial dysfunction unexpectedly causes muscular dystrophy in collagen VI deficiency [Irwin et al (2003) Nat Genet 35, 367-371; Angelin et al. (2007) Proc Natl Acad Sci USA 104, 991-996; Merlini et al. (2008) Proc Natl Acad Sci USA 105, 5225-5229].
His recent identification of the PTP, which forms from dimers of the FOF1 ATP synthase under conditions of oxidative stress [Giorgio et al. (2013) Proc Natl Acad Sci USA 110, 5887-5892; Carraro et al. (2014) J Biol Chem, in press] offers great promise for the molecular definition of pore function in health and disease.
Telethon – Italy;
AIRC (Italian Association on Cancer Research);
University of Padova.