Sustained CaMKII activity mediates transient oxidative stress-induced long-term facilitation of L-type Ca2+ current in cardiomyocytes

Song, Young Hwan; Choi, Eun‐A; Park, Sun Hyun; Lee, Suk Ho; Cho, Hanna; Ho, Won Kyung; Ryu, Shin Young

doi:10.1016/j.freeradbiomed.2011.07.022

Cited by 17 publications

(11 citation statements)

References 39 publications

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“…In the present work it was noticed that prednisolone caused ballooning of the mitochondria with increased electron density of other mitochondria. Some researchers reported that chronic steroid toxicity increases mitochondrial oxidative stress and sensitivity to form the mitochondrial permeability transition pore, which is responsible for mitochondrial swelling due to free passage of molecules, which is a finding similar to ours [27][28][29].…”

Section: Prednisolone and Parsley-treated Rats (Group Iii)supporting

confidence: 85%

Histological study on the possible protective role of parsley oil on prednisolone-induced liver and lung injury in adult male albino rats

Mohammed

Haliem

2013

The Egyptian Journal of Histology

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Section: Prednisolone and Parsley-treated Rats (Group Iii)supporting

confidence: 85%

Histological study on the possible protective role of parsley oil on prednisolone-induced liver and lung injury in adult male albino rats

Mohammed

Haliem

2013

The Egyptian Journal of Histology

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“…Treatment of cultured cardiomyocytes with H 2 O 2 induces increases L-type calcium current (I Ca ) [37], late sodium current (I Na ) [38], and increases diastolic calcium leak from the SR [39], as well as enhances CaMKII oxidation [38]. This increase in I Ca can be partially blocked by reducing agents, CaMKII inhibition, and ATP analogues, and more fully blocked by co-treatment with reducing agents in combination with CaMKII inhibition or ATP analogue [37]. Enhancement of late I Na with H 2 O 2 treatment results in Na + and Ca 2+ overload, early afterdepolarizations (EADs), delayed afterdepolarizations (DADs), and hypercontracture of cardiac myocytes.…”

Section: Arrhythmiamentioning

confidence: 99%

CaMKII oxidative activation and the pathogenesis of cardiac disease

Luczak¹,

Anderson²

2014

Journal of Molecular and Cellular Cardiology

130

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Calcium and redox signaling both play important roles in the pathogenesis of cardiac disease; although how these signals are integrated in the heart remains unclear. One putative sensor for both calcium and oxidative stress in the heart is CaMKII, a calcium activated kinase that has recently been shown to also be regulated by oxidation. Oxidative activation of CaMKII occurs in several models of cardiac disease, including myocardial injury and inflammation, excessive neurohumoral activation, atrial fibrillation, and sinus node dysfunction. Additionally, oxidative activation of CaMKII is suggested in subcellular domains where calcium and ROS signaling intersect, such as mitochondria. This review describes the mechanism of activation of CAMKII by oxidation, the cardiac diseases where oxidized CaMKII has been identified, and suggests contexts where oxidized CaMKII is likely to play an important role.

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“…5) [see reviews (23,73)]. For instance, voltage-gated Ca 2 + channels located at the plasma membrane are phosphorylated by oxidized CaMKII, and Ca 2 + influx from the extracellular space to the cytosol increases (164,165). Ca 2 + release channels at SR/ER, RyR, and inositol 1,4,5-trisphosphate receptors (IP 3 R) are activated by a redoxdependent PTM (73).…”

Section: Mitochondrial Ca 21 Influx Mechanism and Mitochondrial Redoxmentioning

confidence: 99%

Mitochondrial Ion Channels/Transporters as Sensors and Regulators of Cellular Redox Signaling

O‐Uchi

Ryu

Jhun

et al. 2014

Antioxidants & Redox Signaling

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Significance: Mitochondrial ion channels/transporters and the electron transport chain (ETC) serve as key sensors and regulators for cellular redox signaling, the production of reactive oxygen species (ROS) and nitrogen species (RNS) in mitochondria, and balancing cell survival and death. Although the functional and pharmacological characteristics of mitochondrial ion transport mechanisms have been extensively studied for several decades, the majority of the molecular identities that are responsible for these channels/transporters have remained a mystery until very recently. Recent Advances: Recent breakthrough studies uncovered the molecular identities of the diverse array of major mitochondrial ion channels/transporters, including the mitochondrial Ca 2+ uniporter pore, mitochondrial permeability transition pore, and mitochondrial ATP-sensitive K + channel. This new information enables us to form detailed molecular and functional characterizations of mitochondrial ion channels/transporters and their roles in mitochondrial redox signaling. Critical Issues: Redox-mediated post-translational modifications of mitochondrial ion channels/transporters and ETC serve as key mechanisms for the spatiotemporal control of mitochondrial ROS/RNS generation. Future Directions: Identification of detailed molecular mechanisms for redox-mediated regulation of mitochondrial ion channels will enable us to find novel therapeutic targets for many diseases that are associated with cellular redox signaling and mitochondrial ion channels/transporters. Antioxid. Redox Signal. 21, 987-1006.

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Sustained CaMKII activity mediates transient oxidative stress-induced long-term facilitation of L-type Ca2+ current in cardiomyocytes

Cited by 17 publications

References 39 publications

Histological study on the possible protective role of parsley oil on prednisolone-induced liver and lung injury in adult male albino rats

Histological study on the possible protective role of parsley oil on prednisolone-induced liver and lung injury in adult male albino rats

CaMKII oxidative activation and the pathogenesis of cardiac disease

Mitochondrial Ion Channels/Transporters as Sensors and Regulators of Cellular Redox Signaling

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