ArticlePloS one2011
CaMKIIδB mediates aberrant NCX1 expression and the imbalance of NCX1/SERCA in transverse aortic constriction-induced failing heart.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Molecular Mechanisms of L-Type Calcium Channel Dysregulation in Heart Failure.International journal of molecular sciences · 2025Review
- The Dysfunctional Scenario of the Major Components Responsible for Myocardial Calcium Balance in Heart Failure Induced by Aortic Stenosis.Arquivos brasileiros de cardiologia · 2022Article
- Article
- Loss of myeloid differentiation protein 1 promotes atrial fibrillation in heart failure with preserved ejection fraction.ESC heart failure · 2020Article
- Challenges and Opportunities for Therapeutic Targeting of Calmodulin Kinase II in Heart.Frontiers in pharmacology · 2020Review
- Gene Expressions Underlying Mishandled Calcium Clearance and Elevated Generation of Reactive Oxygen Species in the Coronary Artery Smooth Muscle Cells of Chronic Heart Failure Rats.Chinese medical journal · 2017Article
- Effects of Wenxin Keli on Cardiac Hypertrophy and Arrhythmia via Regulation of the Calcium/Calmodulin Dependent Kinase II Signaling Pathway.BioMed research international · 2017Article
- Inhibition of cardiac CaMKII to cure heart failure: step by step towards translation?Basic research in cardiology · 2016Article
- Mitochondrial pathways to cardiac recovery: TFAM.Heart failure reviews · 2016Review
- Calmodulin/CaMKII inhibition improves intercellular communication and impulse propagation in the heart and is antiarrhythmic under conditions when fibrosis is absent.Cardiovascular research · 2016Article
- Protein Phosphatase 1c Associated with the Cardiac Sodium Calcium Exchanger 1 Regulates Its Activity by Dephosphorylating Serine 68-phosphorylated Phospholemman.The Journal of biological chemistry · 2016Article
- Chasing cardiac physiology and pathology down the CaMKII cascade.American journal of physiology. Heart and circulatory physiology · 2015Review
- miR-185 plays an anti-hypertrophic role in the heart via multiple targets in the calcium-signaling pathways.PloS one · 2015Article
- Calcium handling proteins: structure, function, and modulation by exercise.Heart failure reviews · 2014Article
- Toward a hierarchy of mechanisms in CaMKII-mediated arrhythmia.Frontiers in pharmacology · 2014Review
- Article
- CaMKIIdelta subtypes: localization and function.Frontiers in pharmacology · 2014Review
- The promise of CaMKII inhibition for heart disease: preventing heart failure and arrhythmias.Expert opinion on therapeutic targets · 2013Review
- Effects of wenxin keli on the action potential and L-type calcium current in rats with transverse aortic constriction-induced heart failure.Evidence-based complementary and alternative medicine : eCAM · 2013Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca²⁺/calmodulin-dependent protein kinase II δB (CaMKIIδB) is one of the predominant isoforms of CaMKII in the heart. The precise role of CaMKIIδB in the transcriptional cross-talk of Ca²⁺-handling proteins during heart failure remains unclear. In this work, we aim to determine the mechanism of CaMKIIδB in modulating the expression of sarcolemmal Na⁺-Ca²⁺ exchange (NCX1). We also aim to address the potential effects of calmodulin antagonism on the imbalance of NCX1 and sarcoendoplasmic reticulum Ca²⁺ ATPase (SERCA) during heart failure. Eight weeks after transverse aortic constriction (TAC)-induced heart failure in mice, we found that the heart weight/tibia length (HW/TL) ratio and the lung weight/body weight (LW/BW) ratio increased by 59% and 133%, respectively. We further found that the left ventricle-shortening fraction decreased by 40% compared with the sham-operated controls. Immunoblotting revealed that the phosphorylation of CaMKIIδB significantly increased 8 weeks after TAC-induced heart failure. NCX1 protein levels were also elevated, whereas SERCA2 protein levels decreased in the same animal model. Moreover, transfection of active CaMKIIδB significantly increased NCX1 protein levels in adult mouse cardiomyocytes via class IIa histone deacetylase (HDAC)/myocyte enhancer factor-2 (MEF2)-dependent signaling. In addition, pharmacological inhibition of calmodulin/CaMKIIδB activity improved cardiac function in TAC mice, which partially normalized the imbalance between NCX1 and SERCA2. These data identify NCX1 as a cellular target for CaMKIIδB. We also suggest that the CaMKIIδB-induced imbalance between NCX1 and SERCA2 is partially responsible for the disturbance of intracellular Ca²⁺ homeostasis and the pathological process of heart failure.
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