BBA - Molecular Cell Research

BBA - Molecular Cell Research

BBA - Molecular Cell Research
External linkMitochondria and Cardioprotection
Edited by F. Di Lisa, E. Murphy and R. Schulzr
Volume 1813, Issue 7, Pages 1261-1394 (July 2011)

This issue is aimed at reviewing the processes triggered by I/R that alter mitochondria, the signaling pathways that maintain mitochondrial function counteracting myocardial I/R injury, and the pharmacological approaches that act at the mitochondrial level to protect against derangements induced by I/R.

 

Fabio Di Lisa

Fabio Di Lisa is a professor of biochemistry at the University of Padova, Italy. His scientific interest is centered on mitochondria and myofibrillar proteins. After training in studies on heart metabolism, he contributed to the elucidation of the relationships between mitochondrial dysfunction and cell death. In this respect he 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. Moving from the ischemia/reperfusion injury he is now 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.

Dr. Schulz

Dr. Schulz is Professor of Physiology at the Justus-Liebig University of Giessen, Germany. He studied medicine in Düsseldorf, San Diego and Essen and received his MD in 1992. He joined the Institute of Pathophysiology at the University of Essen, Germany where he became assistant professor in 1996 and tenured professor in 2001. Since 2011 he then became Director of the Physiology Institute in Giessen. His research focuses on myocardial ischemia/reperfusion injury (IRI) and protection from it using a translational approach from subcellular particles toward large animal model to define new targets involved in IRI and investigate novel treatment strategies for protecting the heart. More recently, he demonstrated the mitochondrial location of a highly expressed cellular protein (named connexin 43) being essential for cardioprotection. The latter is of utmost importance since a number of human diseases (including genetic variations) are associated with reduced connexin 43 expression.

Dr. Elizabeth Murphy

Dr. Elizabeth Murphy is the Head of the Cardiac Physiology Section in the Systems Biology Center at the National Heart, Lung and Blood Institute. She received her PhD from the University of Pennsylvania in Biochemistry, followed by postdoctoral studies in Physiology at Duke University, before joining the National Institutes of Health. She is an Associated Editor for the Journal of Molecular and Cellular Cardiology, Senior Guest Editor for Circulation and Consulting Editor for Circulation Research. She is a Fellow of the ISHR and the AHA and has previously served as member of the Electrical Signaling, Transport and Arrhythmias and Cardiovascular A NIH Study Sections. She has served on the American Heart Association National Research Committee and the Basic Cardiovascular Science Leadership Committee, and she is President-elect of the American Section of the International Society for Heart Research. She was selected to present the 2009 Keith Reimer Distinguished lecture for the ISHR. Her research is focused on ionic and energetic alterations in cell death and cardioprotection, and the signaling pathways that control these events. Over the years her lab has published a number of critical studies examining the role of ion channel transporters such as the sodium proton and sodium-calcium exchangers in ischemia and reperfusion injury. She has co-authored more than 150 papers and reviews. Her recent work has focused on the role of mitochondria in cell death and cardioprotection.



  
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