2017 - Member of Academia Europaea
His primary areas of study are Mitochondrion, Mitochondrial permeability transition pore, Cell biology, Biochemistry and Cardioprotection. As part of one scientific family, Fabio Di Lisa deals mainly with the area of Mitochondrion, narrowing it down to issues related to the Programmed cell death, and often mitochondrial fusion. His work in Mitochondrial permeability transition pore covers topics such as Mitochondrial membrane transport protein which are related to areas like Pharmacology.
His studies examine the connections between Cell biology and genetics, as well as such issues in Apoptosis, with regards to Arachidonic acid and Thapsigargin. His Biochemistry research includes elements of Biophysics and Calcein. His work carried out in the field of Cardioprotection brings together such families of science as Reperfusion injury, Anesthesia, Intensive care medicine and Ischemic preconditioning.
His main research concerns Mitochondrion, Cell biology, Biochemistry, Internal medicine and Oxidative stress. His Mitochondrion research integrates issues from Cardioprotection, Ischemia, Reactive oxygen species and Programmed cell death, Mitochondrial permeability transition pore. In his study, Cytosol and Calcein is inextricably linked to Biophysics, which falls within the broad field of Mitochondrial permeability transition pore.
His Cell biology research is multidisciplinary, incorporating elements of Apoptosis and Oxidative phosphorylation. His studies deal with areas such as Endocrinology and Cardiology as well as Internal medicine. His Oxidative stress study integrates concerns from other disciplines, such as Oxidation reduction, Disease, Antioxidant and Monoamine oxidase A.
Fabio Di Lisa mostly deals with Mitochondrion, Reactive oxygen species, Cell biology, Oxidative stress and Pharmacology. The concepts of his Mitochondrion study are interwoven with issues in Cardioprotection, Diabetic cardiomyopathy, Programmed cell death and Monoamine oxidase. His Cardioprotection study incorporates themes from Ischemic preconditioning, Heart failure and Mitochondrial permeability transition pore.
His research in Reactive oxygen species intersects with topics in Endogeny, Cyclophilin D and ATP synthase. In his work, ROS formation, Intracellular and Isolated mitochondria is strongly intertwined with Oxidative phosphorylation, which is a subfield of Cell biology. As a member of one scientific family, Fabio Di Lisa mostly works in the field of Oxidative stress, focusing on Oxidation reduction and, on occasion, Risk analysis.
Fabio Di Lisa focuses on Mitochondrion, Reactive oxygen species, Oxidative stress, Cell biology and Diabetic cardiomyopathy. Fabio Di Lisa is involved in the study of Mitochondrion that focuses on Heart metabolism in particular. His Reactive oxygen species study deals with the bigger picture of Biochemistry.
His Oxidative stress study combines topics in areas such as Disease progression, Oxidation reduction and Risk analysis. His Cell biology research is multidisciplinary, incorporating perspectives in Oxidative phosphorylation and Membrane potential. Fabio Di Lisa focuses mostly in the field of Monoamine oxidase, narrowing it down to topics relating to Endoplasmic reticulum and, in certain cases, Endocrinology and Internal medicine.
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Mitochondria and cell death
Paolo Bernardi;Luca Scorrano;Raffaele Colonna;Valeria Petronilli.
FEBS Journal (1999)
Opening of the Mitochondrial Permeability Transition Pore Causes Depletion of Mitochondrial and Cytosolic NAD+and Is a Causative Event in the Death of Myocytes in Postischemic Reperfusion of the Heart
Fabio Di Lisa;Roberta Menabò;Marcella Canton;Maria Barile.
Journal of Biological Chemistry (2001)
The mitochondrial permeability transition from in vitro artifact to disease target
Paolo Bernardi;Alexandra Krauskopf;Emy Basso;Valeria Petronilli.
FEBS Journal (2006)
Postconditioning and protection from reperfusion injury: where do we stand? Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology
Michel Ovize;Gary F. Baxter;Fabio Di Lisa;Péter Ferdinandy.
Cardiovascular Research (2010)
Transient and Long-Lasting Openings of the Mitochondrial Permeability Transition Pore Can Be Monitored Directly in Intact Cells by Changes in Mitochondrial Calcein Fluorescence
Valeria Petronilli;Giovanni Miotto;Marcella Canton;Marisa Brini.
Biophysical Journal (1999)
The Mitochondrial Permeability Transition, Release of Cytochrome c and Cell Death: CORRELATION WITH THE DURATION OF PORE OPENINGS IN SITU
Valeria Petronilli;Daniele Penzo;Luca Scorrano;Paolo Bernardi.
Journal of Biological Chemistry (2001)
A mitochondrial perspective on cell death
Paolo Bernardi;Valeria Petronilli;Fabio Di Lisa;Michael Forte.
Trends in Biochemical Sciences (2001)
Mitochondria and ischemia–reperfusion injury of the heart: Fixing a hole
Fabio Di Lisa;Paolo Bernardi.
Cardiovascular Research (2006)
The mitochondrial permeability transition pore: Molecular nature and role as a target in cardioprotection
Paolo Bernardi;Fabio Di Lisa.
Journal of Molecular and Cellular Cardiology (2015)
Connexin 43 in cardiomyocyte mitochondria and its increase by ischemic preconditioning.
Kerstin Boengler;Giuliano Dodoni;Antonio Rodriguez-Sinovas;Alberto Cabestrero.
Cardiovascular Research (2005)
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