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December 14, 2022Journal of Molecular and Cellular CardiologyOpen Access

Hearts from mice with CaMKII resistant to oxidation at methionines 281/282 (MMVV) had a similar incidence of early ischemia-reperfusion arrhythmias compared to wild type mice.

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Why the study?

Although oxidized CaMKII has been proposed to be important for early ischemia-reperfusion arrhythmias, direct evidence was lacking.

Population

Langendorff-perfused hearts and ventricular cardiomyocytes from C57BL/6 and MMVV mice

Comparison

Isoprenaline, KN93/AIP, NAC, and oxidation-resistant CaMKII (MMVV) vs controls

Design

Preclinical ex vivo and in vitro experimental study

Key result

Hearts from mice with CaMKII resistant to oxidation at methionines 281/282 (MMVV) had a similar incidence of early ischemia-reperfusion arrhythmias compared to wild type mice.

Authors

MHMarie Haugsten HansenMSMani SadrediniAHAlmira Hasic

Discussion

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Overview

Oxidation-resistant CaMKII yields similar early reperfusion arrhythmia rates in mice; leaves open alternative ROS-CaMKII mechanisms for targeted study.

Structured PICO

P
Population
Mice hearts and ventricular cardiomyocytes (wild type and MMVV mutant) exposed to global and simulated ischemia to evaluate early reperfusion arrhythmias.
E
Exposure
Global and simulated ischemia followed by early reperfusion, with or without beta-adrenoceptor stimulation (isoprenaline), CaMKII inhibition (KN93/AIP), or ROS reduction (N-acetylcysteine)
C
Comparator
Wild type mice or untreated controls
O
Outcome
Incidence of early ischemia-reperfusion arrhythmias (IRA) and arrhythmogenic events (Ca2+ waves and sparks)surrogate

Although CaMKII and ROS contribute to early ischemia-reperfusion arrhythmias, oxidation of CaMKII at methionines 281/282 is not a determining factor for these arrhythmias.

Cite This Study

Hansen et al. (2022) studied Early ischemia-reperfusion arrhythmias. CaMKII resistant to oxidation of methionines 281 and 282 (MMVV mutation) vs. Wild type mice (WT) was evaluated on Incidence of early ischemia-reperfusion arrhythmias (IRA). Hearts from mice with CaMKII resistant to oxidation at methionines 281/282 (MMVV) had a similar incidence of early ischemia-reperfusion arrhythmias compared to wild type mice.

synapsesocial.com/papers/6a23d5a9d91ad9240008cd6ahttps://doi.org/10.1016/j.yjmcc.2022.12.002
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Attenuation of ischemia–reperfusion-induced alterations in intracellular Ca2+in cardiomyocytes from hearts treated withN-acetylcysteine andN-mercaptopropionylglycineThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research.2009 · 24 citations
  2. 2Elevated MCU Expression by CaMKIIδB Limits Pathological Cardiac Remodeling2022 · 112 citations
  3. 3SparkMaster: automated calcium spark analysis with ImageJ2007 · 332 citations
  4. 4Targeting CaMKII-δ9 Ameliorates Cardiac Ischemia/Reperfusion Injury by Inhibiting Myocardial Inflammation2022 · 109 citations
  5. 5Oxidized CaMKII causes cardiac sinus node dysfunction in mice2011 · 214 citations