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Prof Martin Crompton
Department of Structural and Molecular Biology
University College London
Gower Street
London
WC1E 6BT
Appointment
  • Emeritus Professor of Biochemistry
  • Div of Biosciences
  • Faculty of Life Sciences
Research Summary
Ischaemic diseases, notably myocardial infarction and stroke, are the leading cause of death and disability throughout the world. Twenty years ago we put forward a mitochondrial model for ischaemia / reperfusion (I/R)injury based on the commonality between factors that induce formation of the permeability transition pore in mitochondria and critical cellular changes in I/R, principally cellular calcium overload, oxidative stress and depleted adenine nucleotides. This led to our identification of cyclosporin A as a potent pore inhibitor able to attenuate I/R injury and of mitochondrial cyclophilin-D as a key component. Current work is aimed at understanding the role of cyclophilin-D in pore formation and on the development of pore inhibitors for use as tools in evaluating permeability transition-mediated mitochondrial dysfunction in cell injury and disease, and as potential therapeutic agents. The cyclophilin work has also been broadened to include the cytosolic isoform, cyclophilin-A, and its role in apoptosis.
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