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Shadi Moghaddas
Researcher at Case Western Reserve University
Publications - 18
Citations - 4167
Shadi Moghaddas is an academic researcher from Case Western Reserve University. The author has contributed to research in topics: Coenzyme Q – cytochrome c reductase & Ischemia. The author has an hindex of 11, co-authored 18 publications receiving 3885 citations. Previous affiliations of Shadi Moghaddas include Veterans Health Administration.
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Journal ArticleDOI
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,Edward J. Lesnefsky +6 more
TL;DR: In this paper, the authors measured reactive oxygen species (ROS) in the mitochondria of Sprague-Dawley rat heart and corresponding submitochondrial particles using the amplex red assay.
Journal ArticleDOI
Function of Mitochondrial Stat3 in Cellular Respiration
Joanna Wegrzyn,Ramesh Potla,Yong Joon Chwae,Naresh Babu V. Sepuri,Qifang Zhang,Thomas Koeck,Marta Derecka,Marta Derecka,Karol Szczepanek,Karol Szczepanek,Magdalena Szelag,Magdalena Szelag,Agnieszka Gornicka,Agnieszka Gornicka,Akira Moh,Shadi Moghaddas,Qun Chen,Santha Bobbili,Joanna Cichy,Jozef Dulak,Darren P. Baker,Alan Wolfman,Dennis J. Stuehr,Dennis J. Stuehr,Medhat O. Hassan,Xin-Yuan Fu,Narayan G. Avadhani,Jennifer I. Drake,Paul Fawcett,Edward J. Lesnefsky,Edward J. Lesnefsky,Andrew C. Larner +31 more
TL;DR: Data indicate that Stat3 is required for optimal function of the ETC, which may allow it to orchestrate responses to cellular homeostasis.
Journal ArticleDOI
Mitochondrial dysfunction in cardiac disease: ischemia--reperfusion, aging, and heart failure.
Edward J. Lesnefsky,Edward J. Lesnefsky,Shadi Moghaddas,Bernard Tandler,Janos Kerner,Charles L. Hoppel,Charles L. Hoppel +6 more
TL;DR: Mechanisms of mitochondrial-derived myocyte injury and the involvement of mitochondria in the pathogenesis of specific cardiac disease states (ischemia, reperfusion, aging, ischemic preconditioning, and cardiomyopathy) are addressed.
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Ischemic defects in the electron transport chain increase the production of reactive oxygen species from isolated rat heart mitochondria
TL;DR: Findings support that mitochondrial damage occurs during ischemia and contributes to myocardial injury during reperfusion and sets the stage for an increase in ROS production during reperFusion as a mechanism of cardiac injury.
Journal ArticleDOI
Blockade of electron transport during ischemia protects cardiac mitochondria.
Edward J. Lesnefsky,Qun Chen,Shadi Moghaddas,Medhat O. Hassan,Bernard Tandler,Charles L. Hoppel +5 more
TL;DR: The limitation of electron flow during ischemia preserves cardiolipin content, cy tochrome c content, and the rate of oxidation through cytochrome oxidase, which contributes to ischemic mitochondrial damage that in turn augments myocyte injury during subsequent reperfusion.