ArticleCell calcium2015
CaMKII-dependent myofilament Ca2+ desensitization contributes to the frequency-dependent acceleration of relaxation.
Article in Cell calcium, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Sex-specific cardiovascular remodeling leads to a divergent sex-dependent development of heart failure in aged hypertensive rats.GeroScience · 2024Article
- The mechano-electric feedback mediates the dual effect of stretch in mouse sinoatrial tissue.Journal of molecular and cellular cardiology plus · 2023Article
- Calcium Signalling in Heart and Vessels: Role of Calmodulin and Downstream Calmodulin-Dependent Protein Kinases.International journal of molecular sciences · 2022Review
- Ion Channel Impairment and Myofilament CaCells · 2021Review
- Effect of transient elevation of glucose on contractile properties in non-diabetic rat cardiac muscle.Heart and vessels · 2021Article
- Article
- Lycium barbarum polysaccharides restore adverse structural remodelling and cardiac contractile dysfunction induced by overexpression of microRNA-1.Journal of cellular and molecular medicine · 2018Article
- SERCA is critical to control the Bowditch effect in the heart.Scientific reports · 2018Article
- Inhibition of calcium/calmodulin-dependent kinase II restores contraction and relaxation in isolated cardiac muscle from type 2 diabetic rats.Cardiovascular diabetology · 2018Article
- Oxidized CaMKII (CaCirculation. Arrhythmia and electrophysiology · 2018Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundPrevious studies suggest that CaMKII activity is required for frequency-dependent acceleration of relaxation (FDAR) in ventricular myocytes. We propose that the underlying mechanism involves CaMKII-dependent regulation of myofilament Ca(2+) sensitivity. METHODS AND
resultsCardiac function was measured in mice using murine echo machine. [Ca(2+)]i and sarcomere length were measured by IonOptix Ca(2+) image system. Increasing pacing rate from 0.5 to 4 Hz in left ventricular myocytes induced frequency-dependent myofilament Ca(2+) desensitization (FDMCD) and FDAR. Acute inhibition of PKA or PKC had no effect, whereas CaMKII inhibition abolished both FDMCD and FDAR. Co-immunoprecipitation of CaMKII and troponin I (TnI) has been detected and CaMKII inhibition significantly reduced serine residue phosphorylation of TnI. Finally, chronic inhibition of CaMKII in vivo reduced TnI phosphorylation and abolished both FDAR and FDMCD, leading to impaired diastolic function.
conclusionsOur results suggest that CaMKII-dependent TnI phosphorylation is involved in FDMCD and the consequent FDAR and that CaMKII inhibition removes this mechanism and thus induces diastolic dysfunction.
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