Paolo Bernardi#
Laudatio by Cesare Montecucco#
Paolo Bernardi had a training of excellence (mitochondrial physiology and ion transport with Giovanni Felice Azzone; cellular and molecular biology with Harvey F. Lodish). After establishing an independent group in 1990, 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 carried out a thorough characterization of the PTP in isolated mitochondria, and defined key points of regulation (membrane potential, matrix pH, Me2+-binding sites, specific redox-sensitive sites).
From the mid 1990s he developed tools to reliably monitor mitochondrial function in situ, which in turn allowed to address mechanistic questions related to PTP operation in intact cells and organs. These advances made it then possible to ask the question of how pharmacological modulation of mitochondrial function in situ can be exploited to force apoptosis in cancer cells and to prevent apoptosis in degenerative diseases, an area that is the current focus of the Bernardi laboratory, His studies on the role of the PTP in disease have been recently extended to in vivo models, and culminated with the demonstration that early mitochondrial adaptation plays a key role in hepatocarcinogenesis by 2-acetylaminof1uorene [Proc Natl Acad Sci USA (2003) 100, 10014-10019]; that TNFα-dependent fulminant hepatitis depends on PTP opening and can be prevented by Cyclosporin A [J Biol Chem (2004) 279, 36803-36808]; and that the muscular dystrophy caused by collagen VI deficiency has an unexpected mitochondrial pathogenesis due to increased PTP opening that can be cured by cyclosporine A [Nat Genet (2003) 35, 367-371; Proc Natl Acad Sci USA (2007) 104, 991-996 and (2008) 105, 5225-5229]. Based on these exciting premises, he is moving on towards the molecular definition of the PTP, the identification of novel mitochondrial drugs, and their rigorous testing in relevant models of disease. His progression from in vitro studies to in vivo models to the experimental therapy of human muscular dystrophy represents a rare case of rigor, creativity and perseverance.
Paolo Bernardi was one of the major actors of the Mitochondrial Renaissance of the 1990s, well before the role of cytochrome c release was discovered as a major mechanism of cell death. As early as 1992, he was one of the very few to realise the importance of mitochondria in cell death, and pioneered the field rapidly reaching international recognition. As of March, 2010 he has published 157 peer-reviewed articles. His publications from 1986 have received 9,350 citations with an h index (n of publications with at least n citations) of 48. His most quoted paper (659 citations, ISI) is an influential review that profoundly affected the long-neglected field of mitochondrial cation transport and the permeability transition [Bernardi (1999) Mitochondrial transport of cations: Channels, exchangers and pemieability transition Physiol Rev 79, 1127-1155]; his most quoted experimental paper (338 citatations, ISI) established a clear link between redox stress and the permeability transition, an issue that turned out to be of key importance in linking oxidative stress to cell death [Petronilli etal. (1994) The voltage sensor of the mitochondrial permeability transition pore is tuned by the oxidation-reduction state of vicinal thiols. Increase of the gating potential by oxidants and its reversal by reducing agents. J Biol Chem 269, 16638-16642].
Paolo Bernardi is a recognized international leader. He has been invited to give 138 lectures at international meetings and 100 seminars at prestigious Institutions worldwide. He has organized or coorganized key meetings on mitochondrial pathophysiology that significantly contributed to the now continuing success of the field (New Perspectives in Mitochondrial Research, Padova 1993; Colloquium The Mitochondrial Permeability Transition in Accidental and Programmed Cell Death, 9th European Bioenergetics Conference, Louvain-la-Neuve 1996; Albany Conference Frontiers in Mitochondrial Research, Albany 1996; New Perspectives in Mitochondrial Research, Padova 1997; 2nd Albany Conference Frontiers in Mitochondrial Research, Albany 1998; 3rd Albany Conference Frontiers in Mitochondrial Research, Albany 2000; New Frontiers in Mitochondrial Research – from Bioenergetics to Dynamics, Bertinoro 2007; 52nd Annual Meeting of the Biophysical Society USA, Bioenergetics Subgroup Meeting Mitochondria Bioenergetics in Disease and Therapeutics, Long Beach 2008, 54th Annual Meeting of the Biophysical Society USA, Bioenergetics Subgroup Meeting Mitochondria in Disease, San Francisco 2010).
He has been Guest Editor of the Special Issues of Biochimica et Biophysica Acta "Mitochondria in Cell Death" (1998), BioFactors "New Perspectives in Mitochondrial Research" (1998), and IUBMB LW “Perspectives in Mitochondrial Research" (2001).
He serves or has served in the Editorial Boards of the Journal of Biological Chemistry (1997 2002, 2003-2008, 2010-present), Archives of Biochemistry and Biophysics (1998-2003), Biochimica et Biophysica Acta (l999-present), and IUBMB Life (2002-2007).
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