E
Elizabeth D. Luczak
Researcher at Johns Hopkins University School of Medicine
Publications - 36
Citations - 2667
Elizabeth D. Luczak is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Ca2+/calmodulin-dependent protein kinase & Medicine. The author has an hindex of 17, co-authored 29 publications receiving 2226 citations. Previous affiliations of Elizabeth D. Luczak include University of Colorado Boulder & University of Iowa.
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Journal ArticleDOI
Corrigendum: The mitochondrial uniporter controls fight or flight heart rate increases
Yuejin Wu,Tyler P. Rasmussen,Olha M. Koval,Mei Ling A. Joiner,Duane D. Hall,Biyi Chen,Elizabeth D. Luczak,Qiongling Wang,Adam G. Rokita,Xander H.T. Wehrens,Long-Sheng Song,Mark E. Anderson +11 more
TL;DR: In this paper, the y axis values were wrongly given as 0, 20, 40, 60 and 80 in the middle and the lower panels, respectively, in Fig. 4c of this article.
Journal ArticleDOI
CaMKII determines mitochondrial stress responses in heart
Mei Ling A. Joiner,Olha M. Koval,Jingdong Li,Jingdong Li,B. Julie He,Chantal Allamargot,Zhan Gao,Elizabeth D. Luczak,Duane D. Hall,Brian D. Fink,Biyi Chen,Jinying Yang,Steven A. Moore,Thomas D. Scholz,Stefan Strack,Peter J. Mohler,Peter J. Mohler,William I. Sivitz,William I. Sivitz,Long-Sheng Song,Mark E. Anderson +20 more
TL;DR: CaMKII activity is identified as a central mechanism for mitochondrial Ca2+ entry in myocardial cell death, and indicates that mitochondrial-targeted CaMKII inhibition could prevent or reduce myocardials death and heart failure in response to common experimental forms of pathophysiological stress.
Journal ArticleDOI
Oxidized Ca(2+)/calmodulin-dependent protein kinase II triggers atrial fibrillation.
Anil Purohit,Adam G. Rokita,Xiaoqun Guan,Biyi Chen,Olha M. Koval,Niels Voigt,Niels Voigt,Stefan Neef,Thomas Sowa,Zhan Gao,Elizabeth D. Luczak,Hrafnhildur Stefansdottir,Andrew C. Behunin,Na Li,Ramzi N. El-Accaoui,Baoli Yang,Paari Dominic Swaminathan,Robert M. Weiss,Xander H.T. Wehrens,Long-Sheng Song,Dobromir Dobrev,Dobromir Dobrev,Lars S. Maier,Mark E. Anderson,Mark E. Anderson +24 more
TL;DR: CaMKII is a molecular signal that couples increased reactive oxygen species with AF and that therapeutic strategies to decrease oxidized CaMKII may prevent or reduce AF.
Journal ArticleDOI
Oxidation of CaMKII determines the cardiotoxic effects of aldosterone
B. Julie He,Mei Ling A. Joiner,Madhu V. Singh,Elizabeth D. Luczak,Paari Dominic Swaminathan,Olha M. Koval,William J. Kutschke,Chantal Allamargot,Jinying Yang,Xiaoqun Guan,Kathy Zimmerman,Isabella M. Grumbach,Robert M. Weiss,Douglas R. Spitz,Curt D. Sigmund,W. Matthijs Blankesteijn,Stephane Heymans,Stephane Heymans,Peter J. Mohler,Mark E. Anderson +19 more
TL;DR: It is shown that oxidized myocardial CaMKII mediates the cardiotoxic effects of aldosterone on the cardiac matrix and establish CaMK II as a nodal signal for the neurohumoral pathways associated with poor outcomes after myocardia infarction.
Journal ArticleDOI
Diabetes increases mortality after myocardial infarction by oxidizing CaMKII.
Min Luo,Xiaoqun Guan,Elizabeth D. Luczak,Di Lang,William Kutschke,Zhan Gao,Jinying Yang,Patric Glynn,Samuel Sossalla,Paari Dominic Swaminathan,Robert M. Weiss,Baoli Yang,Adam G. Rokita,Adam G. Rokita,Lars S. Maier,Igor R. Efimov,Thomas J. Hund,Mark E. Anderson +17 more
TL;DR: The findings suggest that activation of a mitochondrial/ox-CaMKII pathway contributes to increased sudden death in diabetic patients after myocardial infarction.