M
Mark E. Anderson
Researcher at Johns Hopkins University School of Medicine
Publications - 307
Citations - 20458
Mark E. Anderson 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 72, co-authored 252 publications receiving 17510 citations. Previous affiliations of Mark E. Anderson include Vanderbilt University & University of Colorado Denver.
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Journal ArticleDOI
The cVAD registry for percutaneous temporary hemodynamic support: A prospective registry of Impella mechanical circulatory support use in high-risk PCI, cardiogenic shock, and decompensated heart failure
George W. Vetrovec,Mark E. Anderson,Theodore Schreiber,Jeffrey J. Popma,William Lombardi,Brijeshwar Maini,Jacob E. Møller,Andreas Schäfer,Simon R. Dixon,Shelley A. Hall,E. Magnus Ohman,Catalin Mindrescu,Jeffrey W. Moses,William W. O'Neill +13 more
TL;DR: The upgraded catheter-based ventricular assist devices registry will provide a more robust opportunity to assess acute and late outcomes of current and future device use worldwide, and provide a mechanism for postmarketing surveillance.
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Ca2+-dependent regulation of cardiac L-type Ca2+ channels: Is a unifying mechanism at hand?
TL;DR: A recent explosion of work has shed new light on the mechanisms and molecular identity of domains necessary for [Ca2+]i-dependent regulation of LTCC.
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Reduced repolarization reserve in ventricular myocytes from female mice
TL;DR: Ventricular action potential repolarization is prolonged in myocytes from female compared to male mice and female mice have reduced RR that is unmasked by FK506, suggesting that gender is an important variable for cardiovascular studies using mice.
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BK channels regulate sinoatrial node firing rate and cardiac pacing in vivo
Michael H. Lai,Yuejin Wu,Zhan Gao,Mark E. Anderson,Julie E. Dalziel,Andrea L. Meredith,Andrea L. Meredith +6 more
TL;DR: It is demonstrated that loss of BK current decreases SANC automaticity, consistent with slowed sinus pacing after PAX injection in vivo, and suggest BK channels are potential therapeutic targets for disorders of heart rate.
Journal ArticleDOI
Stress Signaling JNK2 Crosstalk With CaMKII Underlies Enhanced Atrial Arrhythmogenesis.
Jiajie Yan,Weiwei Zhao,Justin K. Thomson,Xianlong Gao,Dominic DeMarco,Elena Carrillo,Biyi Chen,Xiaomin Wu,Kenneth S. Ginsburg,Mamdouh Bakhos,Donald M. Bers,Mark E. Anderson,Long-Sheng Song,Michael Fill,Xun Ai +14 more
TL;DR: JNK2-driven CaMKII activation is identified as a novel mode of kinase crosstalk and a causal factor in atrial arrhythmic remodeling, making JNK2 a compelling new therapeutic target for AF prevention and treatment.