CaMKII in myocardial hypertrophy and heart failure.
TLDR
The molecular physiology ofCaMKII is introduced and the impact of CaMKII on ion channels, Ca handling proteins and transcription in myocardium is discussed, which appears to reduce arrhythmias and improve myocardial responses to pathological stimuli.About:
This article is published in Journal of Molecular and Cellular Cardiology.The article was published on 2011-10-01 and is currently open access. It has received 402 citations till now. The article focuses on the topics: Ca2+/calmodulin-dependent protein kinase & Muscle hypertrophy.read more
Citations
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Journal ArticleDOI
Diabetic hyperglycaemia activates CaMKII and arrhythmias by O-linked glycosylation
Jeffrey R. Erickson,Laetitia Pereira,Lianguo Wang,Guanghui Han,Amanda Ferguson,Khanha Dao,Ronald J. Copeland,Florin Despa,Florin Despa,Gerald W. Hart,Crystal M. Ripplinger,Donald M. Bers +11 more
TL;DR: O-GlcNAc modification of CaMKII is a novel signalling event in pathways that may contribute critically to cardiac and neuronal pathophysiology in diabetes and other diseases.
Journal ArticleDOI
Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets.
Yow Keat Tham,Yow Keat Tham,Bianca C. Bernardo,Jenny Y. Y. Ooi,Kate L. Weeks,Julie R. McMullen,Julie R. McMullen +6 more
TL;DR: New therapeutic approaches either entering clinical trials or in preclinical development, and the challenges that remain in translating these discoveries to new and approved therapies for heart failure are addressed.
Journal ArticleDOI
Signaling effectors underlying pathologic growth and remodeling of the heart
TL;DR: In this article, the authors discuss therapeutic avenues emerging from molecular and genetic studies of cardiovascular disease in animal models, and focus on selected therapeutic targets that have more recently emerged and have a tangible translational potential given the available pharmacologic agents that could be readily evaluated in human clinical trials.
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
Mechanisms of altered Ca2+ handling in heart failure
Min Luo,Mark E. Anderson +1 more
TL;DR: This review focuses on the molecular mechanisms of defective Ca2+ cycling in heart failure and considers how fundamental understanding of these pathways may translate into novel and innovative therapies.
References
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Journal ArticleDOI
Sensitivity of CaM Kinase II to the Frequency of Ca2+ Oscillations
Paul De Koninck,Howard Schulman +1 more
TL;DR: Rapid superfusion of immobilized Ca2+- and calmodulin-dependent protein kinase II in vitro showed that the enzyme can decode the frequency ofCa2+ spikes into distinct amounts of kinase activity, suggesting its pivotal role in activity-dependent forms of synaptic plasticity.
Journal ArticleDOI
A dynamic pathway for calcium-independent activation of CaMKII by methionine oxidation
Jeffrey R. Erickson,Mei Ling A. Joiner,Xiaoqun Guan,William Kutschke,Jinying Yang,Carmine V. Oddis,Ryan K. Bartlett,John S. Lowe,Susan E. O'Donnell,Nukhet Aykin-Burns,Matthew C. Zimmerman,Kathy Zimmerman,Amy-Joan L. Ham,Robert M. Weiss,Douglas R. Spitz,Madeline A. Shea,Roger J. Colbran,Peter J. Mohler,Mark E. Anderson +18 more
TL;DR: It is shown that oxidation of paired regulatory domain methionine residues sustains CaMKII activity in the absence of Ca2+/CaM and highlights the critical importance of oxidation-dependent CaMK II activation to AngII and ischemic myocardial apoptosis.
Journal ArticleDOI
Class II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy
Chun Li Zhang,Timothy A. McKinsey,Shurong Chang,Christopher L. Antos,Joseph A. Hill,Eric N. Olson +5 more
TL;DR: It is shown that class II HDACs are substrates for a stress-responsive kinase specific for conserved serines that regulate MEF2-HDAC interactions, and act as signal-responsive suppressors of the transcriptional program governing cardiac hypertrophy and heart failure.
Journal ArticleDOI
Ca2+/Calmodulin–Dependent Protein Kinase Modulates Cardiac Ryanodine Receptor Phosphorylation and Sarcoplasmic Reticulum Ca2+ Leak in Heart Failure
TL;DR: The results suggest that CaMKII-dependent phosphorylation of RyR2 is involved in enhanced SR diastolic Ca leak and reduced SR Ca load in HF, and may thus contribute to arrhythmias and contractile dysfunction in HF.
Journal ArticleDOI
Methionine sulfoxide reductase (MsrA) is a regulator of antioxidant defense and lifespan in mammals.
Jackob Moskovitz,Shoshana Bar-Noy,Wesley M. Williams,Jesús R. Requena,Barbara S. Berlett,Earl R. Stadtman +5 more
TL;DR: It seems that MsrA may play an important role in aging and neurological disorders.
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