D
Donald M. Bers
Researcher at University of California, Davis
Publications - 607
Citations - 57349
Donald M. Bers is an academic researcher from University of California, Davis. The author has contributed to research in topics: Ryanodine receptor & Ca2+/calmodulin-dependent protein kinase. The author has an hindex of 118, co-authored 570 publications receiving 52757 citations. Previous affiliations of Donald M. Bers include University of Maryland, Baltimore & Loyola University Medical Center.
Papers
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Journal ArticleDOI
Cardiac excitation–contraction coupling
TL;DR: Of the ions involved in the intricate workings of the heart, calcium is considered perhaps the most important and spatial microdomains within the cell are important in localizing the molecular players that orchestrate cardiac function.
Journal ArticleDOI
Excitation-Contraction Coupling and Cardiac Contractile Force.
Donald M. Bers,Yujie Zhu +1 more
TL;DR: The major cellular structures involved in E-C coupling include myofilaments, Na/Ca exchange and the sarcolemmal Ca-pump as mentioned in this paper, as well as the sources and sinks of activator calcium.
Journal ArticleDOI
Calcium cycling and signaling in cardiac myocytes.
TL;DR: This review focuses on Ca signaling in cardiac myocytes as pertaining to electrophysiology, excitation-contraction coupling, modulation of contractile function, energy supply-demand balance, cell death, and transcription regulation.
Book
Excitation-Contraction Coupling and Cardiac Contractile Force
TL;DR: A large number of the major cellular structures involved in E-C coupling, including myofilaments, are involved in cardiac contraction by SR and sarcolemmal Ca fluxes, and Ca inotropy and Ca mismanagement is studied.
Journal ArticleDOI
Arrhythmogenesis and contractile dysfunction in heart failure: Roles of sodium-calcium exchange, inward rectifier potassium current, and residual beta-adrenergic responsiveness.
TL;DR: Data is presented to support a novel paradigm in which changes in NaCaX and IK1, and residual &bgr;-AR responsiveness, conspire to greatly increase the propensity for triggered arrhythmias in HF.