2018
DOI: 10.21037/jtd.2018.11.01
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Mitochondria in β-adrenergic signaling: emerging therapeutic perspectives in heart failure and ventricular arrhythmias

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Cited by 4 publications
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“…Christos Kontogiannis et al found that anthracyclines selectively bind to endogenous cardiolipin in mitochondria, resulting in mitochondrial accumulation and disruption of the electron transport chain via inhibition of mitochondrial complexes I and II; these effects result in additional ROS production and cardiolipin peroxidation. Mitochondrial damage can mediate the increase in calcium load and ROS production induced by adrenaline signaling and can induce the phosphorylation of the ryanodine receptor, leading to sarcoplasmic reticulum Ca2+ leakage, which leads to arrhythmia [ 21 ]. Additionally, anthracycline-based drugs can be mediated by reactive oxygen species groups, and free-state iron complex formation, and in the process, iron can generate ROS.…”
Section: Discussionmentioning
confidence: 99%
“…Christos Kontogiannis et al found that anthracyclines selectively bind to endogenous cardiolipin in mitochondria, resulting in mitochondrial accumulation and disruption of the electron transport chain via inhibition of mitochondrial complexes I and II; these effects result in additional ROS production and cardiolipin peroxidation. Mitochondrial damage can mediate the increase in calcium load and ROS production induced by adrenaline signaling and can induce the phosphorylation of the ryanodine receptor, leading to sarcoplasmic reticulum Ca2+ leakage, which leads to arrhythmia [ 21 ]. Additionally, anthracycline-based drugs can be mediated by reactive oxygen species groups, and free-state iron complex formation, and in the process, iron can generate ROS.…”
Section: Discussionmentioning
confidence: 99%