Edward J. Lesnefsky mainly focuses on Mitochondrion, Ischemia, Oxidative phosphorylation, Biochemistry and Cytochrome c. When carried out as part of a general Mitochondrion research project, his work on Heart metabolism is frequently linked to work in Cardiolipin, therefore connecting diverse disciplines of study. The Ischemia portion of his research involves studies in Cardiology and Internal medicine.
In his work, Myocardial ischemia, Neuroscience, Mitochondrial fission, Mitophagy and Carbohydrate metabolism is strongly intertwined with Programmed cell death, which is a subfield of Oxidative phosphorylation. His Cytochrome c study combines topics from a wide range of disciplines, such as Anesthesia, Biophysics, Respiratory function, Respiratory chain and Pharmacology. His research in the fields of STAT3 and Senescence overlaps with other disciplines such as Genomics.
Edward J. Lesnefsky spends much of his time researching Mitochondrion, Ischemia, Internal medicine, Biochemistry and Oxidative phosphorylation. His Mitochondrion research is classified as research in Cell biology. In general Cell biology study, his work on STAT3 and Signal transduction often relates to the realm of Apoptosis-inducing factor, thereby connecting several areas of interest.
His research in Ischemia intersects with topics in Anesthesia and Pharmacology. His Internal medicine study incorporates themes from Mitochondrial biogenesis, Endocrinology, Surgery and Cardiology. Edward J. Lesnefsky interconnects Myofibril and Programmed cell death in the investigation of issues within Oxidative phosphorylation.
His primary areas of investigation include Mitochondrion, Internal medicine, Cell biology, Oxidative phosphorylation and Ischemia. His Mitochondrion research incorporates elements of Electron transport chain, Heart failure, Beta oxidation, Endoplasmic reticulum and Programmed cell death. His Internal medicine research integrates issues from Endocrinology, Perioperative and Cardiology.
His research on Cell biology also deals with topics like
The scientist’s investigation covers issues in Mitochondrion, Ischemia, Oxidative phosphorylation, Reactive oxygen species and Cell biology. Edward J. Lesnefsky combines subjects such as Metformin, Electron transport chain, Endocrinology, Internal medicine and Programmed cell death with his study of Mitochondrion. The study incorporates disciplines such as Beta oxidation and Biochemistry in addition to Ischemia.
His work on Mitochondrial membrane transport protein and Gene knockdown as part of general Biochemistry research is frequently linked to Tafazzin, bridging the gap between disciplines. Edward J. Lesnefsky performs multidisciplinary studies into Oxidative phosphorylation and Cardiolipin in his work. The various areas that Edward J. Lesnefsky examines in his Cell biology study include Calpain and Mitophagy.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Production of Reactive Oxygen Species by Mitochondria: CENTRAL ROLE OF COMPLEX III *
Qun Chen;Qun Chen;Edwin J. Vazquez;Shadi Moghaddas;Charles L. Hoppel;Charles L. Hoppel.
Journal of Biological Chemistry (2003)
Function of Mitochondrial Stat3 in Cellular Respiration
Joanna Wegrzyn;Ramesh Potla;Yong Joon Chwae;Naresh B.V. Sepuri.
Science (2009)
Mitochondrial dysfunction in cardiac disease: ischemia--reperfusion, aging, and heart failure.
Edward J. Lesnefsky;Edward J. Lesnefsky;Shadi Moghaddas;Bernard Tandler;Janos Kerner.
Journal of Molecular and Cellular Cardiology (2001)
Intracoronary ultrasound imaging: Correlation of plaque morphology with angiography, clinical syndrome and procedural results in patients undergoing coronary angioplasty
John McB. Hodgson;Karan G. Reddy;Randeep Suneja;Ravi N. Nair.
Journal of the American College of Cardiology (1993)
Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria
Qun Chen;Shadi Moghaddas;Charles L. Hoppel;Edward J. Lesnefsky.
American Journal of Physiology-cell Physiology (2008)
Sphingosine-1-phosphate produced by sphingosine kinase 2 in mitochondria interacts with prohibitin 2 to regulate complex IV assembly and respiration
Graham M. Strub;Melanie Paillard;Jie Liang;Ludovic Gomez.
The FASEB Journal (2011)
Modulation of electron transport protects cardiac mitochondria and decreases myocardial injury during ischemia and reperfusion
Qun Chen;Amadou K. S. Camara;David F. Stowe;David F. Stowe;David F. Stowe;Charles L. Hoppel.
American Journal of Physiology-cell Physiology (2007)
Myocardial ischemia decreases oxidative phosphorylation through cytochrome oxidase in subsarcolemmal mitochondria
Edward J. Lesnefsky;Bernaed Tandler;Jian Ye;Thomas J. Slabe.
American Journal of Physiology-heart and Circulatory Physiology (1997)
Aging selectively decreases oxidative capacity in rat heart interfibrillar mitochondria.
Stephen W. Fannin;Edward J. Lesnefsky;Thomas J. Slabe;Mehat O. Hassan.
Archives of Biochemistry and Biophysics (1999)
Blockade of electron transport during ischemia protects cardiac mitochondria.
Edward J. Lesnefsky;Qun Chen;Shadi Moghaddas;Medhat O. Hassan.
Journal of Biological Chemistry (2004)
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