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  • Nipavan Chiamvimonvat
    Correspondence
    Address reprint requests and correspondence: Dr Nipavan Chiamvimonvat, Department of Internal Medicine and Pharmacology, University of California, Davis, GBSF 6315, 451 Health Sciences Dr, Davis, CA 95616.
    Affiliations
    Department of Internal Medicine and Pharmacology, University of California, Davis, Davis, California
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Published:February 09, 2021DOI:https://doi.org/10.1016/j.hrthm.2021.02.005
      In the current study, Liu et al (Circ Res 2021, https://doi.org/10.1161/CIRCRESAHA.120.318562, PMID 33522833) tested whether moderate mitochondrial Ca2+ uniporter (MCU) overexpression is beneficial or detrimental in the development of heart failure (HF) and arrhythmias in a guinea pig model (ACi) of HF and sudden cardiac death (SCD). In vivo viral gene transfer was used to increase MCU levels by ∼30% in ACi hearts, leading to an increase in mitochondrial Ca2+ uptake, decreased oxidative stress, and increased β-adrenergic– and frequency-dependent enhancement of Ca2+ transients and contractions. In addition, MCU overexpression decreased sarcoplasmic reticulum (SR) Ca2+ leak in the ACi group and normalized β-adrenergic responses. In vivo studies demonstrated that MCU overexpression in the ACi heart decreased pulmonary edema and interstitial fibrosis and prevented triggered arrhythmias. The authors conclude that moderate MCU overexpression in failing hearts enhances contractility and responses to β-adrenergic stimulation and prevents cardiac arrhythmias by inhibiting mitochondrial oxidative stress-induced SR Ca2+ leak.
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