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Elizabeth Murphy: North American Coordinator

Elizabeth Murphy received her B.A. in 1974 and her Ph.D. in biochemistry in 1980 from the University of Pennsylvania. Before joining the NHLBI in 2006 as the head of the Cardiac Physiology Section, she was the head of the Cell Biology Group at the National Institute of Environmental Health Sciences. Dr. Murphy’s laboratory studies the molecular mechanisms involved in cardiac cell death, as well as the mechanisms that protect the heart against damage. The knowledge gained from these studies may help identify novel therapies to reduce cardiac injury during ischemia and reperfusion. The current dogma suggests that calcium overload and reactive oxygen species generated during ischemia and heart failure lead to activation of a mitochondrial pore (mPTP) which initiates cell death. To better understand the regulation of the mPTP her lab has studied the mechanisms regulated by cyclophilin D, the only currently established member (albeit a regulator) of the mPTP. These studies demonstrated that cyclophilin D regulates mitochondrial acetylation. 

National Institutes of Health USA

Michel Ovize: European Coordinator

Michel Ovize received his Medical degree from the Claude Bernard university of Lyon (France) in 1990, his PhD in 1993 and became a full Professor of Physiology in 1998. He has been trained as a (interventional) cardiologist and is currently head of the non-invasive and stress testing cardiology department at the Louis Pradel Hospital, head of the INSERM “cardioprotection” team and coordinator of the “Organ Protection” Institute in Lyon.  He has been working for several years on the detrimental effects of cardiac ischemia-reperfusion injury and cardioprotective strategies from bench to bedside. He has contributed to our understanding of the role of mitochondria in reperfusion injury and has conducted several clinical trials to improve patients’ clinical outcomes in the context of myocardial infarction.   

CarMeN Laboratory,
Université Claude Bernard, Lyon , France

Paolo Bernardi

Paolo received his Medical Degree from the University of Padova in 1978 and has been a full Professor there since 2000, where he has been the Deputy Dean of the Medical Faculty and the Director of the Department of Biomedical Sciences, and is presently the Coordinator of the PhD programme. He pioneered the field of mitochondrial channels and their role in cellular pathophysiology, in particular 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 (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. The recent identification of the PTP, which appears to originate from dimers of the FOF1 ATP synthase, offers great promise for further definition of its function in health and disease.

University of Padova, Italy

Fabio Di Lisa

Fabio Di Lisa is Professor of Biochemistry at the University of Padova. He received his Medical Degree from the Catholic University in Rome in 1977 and became Board certified in Cardiology in 1980. His team’s research is centered on mitochondria and myofibrillar proteins of the heart. To this aim they have contributed to the elucidation of the relationships between mitochondrial dysfunction and cell death. In a fruitful collaboration with the laboratory of Prof. Bernardi we characterized the involvement of the permeability transition pore in myocardial ischemia by developing methods that are currently used in studies in isolated cells and intact hearts. These methods were also exploited for characterizing novel aspects of photosensitizers used for photodynamic therapy, a field of research with a long standing tradition at the University of Padova. Moving from the ischemia/reperfusion injury he is currently focusing on the role of mitochondria in heart failure by characterizing processes involved in the mitochondrial formation of reactive oxygen species as causative factors of permeability transition and myofilament derangements.

University of Padova, Italy

Michael Cohen

Michael Cohen is an Associate Professor of Physiology and Pharmacology at the Oregon Health and Science University. He obtained his BS in Chemistry from the University of California, Irvine and his PhD from UCSF in Chemical Biology, he also performed postdoctoral work at Cornell and is a Pew Biomedical Scholar. His current research aims to understand the role of nicotinamide adenine dinucleotide (NAD+) in cell signaling. In addition to its well-known role as a co-factor in redox metabolism, NAD+ is used as a substrate for posttranslational modifications. He is also combining chemistry and molecular design to develop selective inhibitors of biochemical processes including the PTP.

Oregon Heath and Science University, USA

Jeffery Molkentin

Dr. Molkentin is a Professor of pediatrics at Cincinnati Children's Hospital Medical Center in the United States of America where he first joined as faculty in 1997.  He has also been an Investigator of the Howard Hughes Medical Institute (HHMI) since 2008. He obtained his BS in Biology from Marquette University in Milwaukee Wisconsin (USA) and his PhD in Physiology from the Medical College of Wisconsin (USA). His current research focuses on understanding the molecular mechanisms of heart and skeletal muscle disease, with a special interest in mitochondrial-dependent mechanisms of nonapoptotic death such as mitochondrial permeability transition pore (MPTP) formation that underlies cellular necrosis. Prominent diseases of both heart and skeletal muscle are affected by cellular necrosis mediated by the MPTP, so identifying the genes that further control this process could have a substantial effect on our treatment of these types of diseases, which is a goal of the Leducq project. We are also interested in characterizing the intracellular signaling pathways that control cellular growth, differentiation and cell death in cardiac and skeletal muscle. A better understanding of the signaling pathways that control these processes, coupled with the identification of novel genes, could suggest new treatment strategies for human heart disease.

Cincinnati Children's Hospital Medical Center, USA

Gyorgy Hajnoczky

Gyorgy received his MD from Semmelweis Medical University in 1987 and PhD from the Hungarian National Academy of Sciences in 1994. He has been a Full Professor at Thomas Jefferson University since 2002, where he also has served as the founding director of the MitoCare Center for Mitochondrial Imaging Research and Diagnostics. The long term objective of his group is to reveal critical roles mitochondria play in integrating cell and tissue function through their dynamics and interactions with other cell structures, coordinating calcium homeostasis, integrating cell metabolism, exerting cellular quality control, and driving cell life/death decisions. The Hajnoczky group has 20+ years of experience in the study of mitochondrial signaling and dynamics and has provided evidence on the control of both ATP production and apoptosis induction by calcium oscillations. His group demonstrated direct physical linkage (tethering) and local calcium transfer between endoplasmic reticulum and mitochondria and also made contributions to the research on mitochondrial fusion and motility dynamics. Gyorgy was also instrumental in setting up many imaging approaches and in designing some molecular tools which are currently widely used in mitochondrial biology research.

Thomas Jefferson University

Jonathan Dando

Jonathan Dando is the Managing Director of Echino Limited; a company that specialises in optimising and implementing global collaborations and R&D portfolios in the health and medicial devices sector. He has a BSc in Biophysics from the University of Portsmouth, UK, and received his PhD in Genetic Engineering from the UK Open University, which he performed in Milan, Italy. He has worked all over the planet for small and large biopharmaceutial companies, technology transfer companies, research institutes and Universities and in partnerships composed of these stakeholders. He has directed several large portfolios focused on developing insight and therapeutic options for a wide array of age related and degenerative diseases, with a specific focus on cardiovascular, neuromuscular disorders and soft tissue disorders. He has also established many companies which have been spin-off biotech/medical device companies from the research outcomes of the portfolios.

Echino Ltd

Michael Forte (Alumni)

Michael Forte was a member of Mitocardia from its inception to early 2019 and was a senior scientist at the Vollum Institute and a professor in the Departments of Molecular and Medical Genetics, Cell and Developmental Biology, and Physiology and Pharmacology in the School of Medicine. After being awarded his B.S. from the University of Notre Dame in 1973, Forte earned his Ph.D. in Genetics from the University of Washington in 1978. The Forte lab is investigating the role of mitochondria in the overall regulation of cellular calcium (Ca2+). Ca2+ ions probably represent the most ubiquitous signaling pathway in all cells. Mitochondria are now recognized as initiators and transducers of a range of cell signals, participating in neuronal functions like synaptic plasticity and processes central to activation and amplification of programmed cell death. Moreover, as the main source of cellular ATP, mitochondria must respond to fluctuating energy demands of the cell. As local and global fluctuations in Ca2+ concentration are ubiquitous in eukaryotic cells and are the common factor in a wide array of intra- and inter-cellular signaling cascades, the relationships between mitochondrial function and Ca2+ transients is currently a subject of intense scrutiny. The mitochondrial Ca2+ pool oscillates rapidly in synchrony with cytosolic Ca2+ and thus, mitochondria have the ability to shape cytosolic Ca2+ transients. Mitochondria also respond to Ca2+ uptake by upregulating energy production, thus integrating metabolism with local Ca2+ signaling. The Forte lab is interested in the reciprocal effects of Ca2+ on mitochondria and mitochondria on the Ca2+ signals. Through genetic and drug discovery approaches, the goal is to understand the response of mitochondria to Ca2+, the pathways by which Ca2+ accumulates into mitochondria, and the potential role of mitochondrial Ca2+ particularly in cardiovascular disease processes.

Mike retired after an illustrious career in Academia and Research in early 2019, being replaced by Gyorgy Hajnoczky and his team.

Oregon Heath and Science University, USA

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