2013
DOI: 10.1161/circulationaha.113.003313
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Abstract: Background Atrial fibrillation is a growing public health problem without adequate therapies. Angiotensin II (Ang II) and reactive oxygen species (ROS) are validated risk factors for atrial fibrillation (AF) in patients, but the molecular pathway(s) connecting ROS and AF is unknown. The Ca2+/calmodulin-dependent protein kinase II (CaMKII) has recently emerged as a ROS activated proarrhythmic signal, so we hypothesized that oxidized CaMKIIδ(ox-CaMKII) could contribute to AF. Methods and Results We found ox-Ca… Show more

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Cited by 252 publications
(230 citation statements)
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“…Genomic analyses showed that genes that were uniquely up regulated in patients with no POAF were mostly supported by reduction reactions suggesting that the overall redox balance favors anti-oxidant state in these patients resistant to POAF [3]. Indeed, mice lacking critical oxidation sites in CaMKII or mice over expressing methionine sulfoxide reductase A, an enzyme that reduces oxidized CaMKII, are resistant to oxidative AF evaluated by programmed electrical stimulation [10]. Recent clinical studies showed that POAF originated from the LA and not from the pulmonary veins (PVs) [36,37] as in the present study.…”
Section: Discussionmentioning
confidence: 99%
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“…Genomic analyses showed that genes that were uniquely up regulated in patients with no POAF were mostly supported by reduction reactions suggesting that the overall redox balance favors anti-oxidant state in these patients resistant to POAF [3]. Indeed, mice lacking critical oxidation sites in CaMKII or mice over expressing methionine sulfoxide reductase A, an enzyme that reduces oxidized CaMKII, are resistant to oxidative AF evaluated by programmed electrical stimulation [10]. Recent clinical studies showed that POAF originated from the LA and not from the pulmonary veins (PVs) [36,37] as in the present study.…”
Section: Discussionmentioning
confidence: 99%
“…Increased systemic and atrial myocardial oxidative stress is often observed in post-operative patients with new onset (acute) paroxysmal AF (POAF) [3,4] with an incidence of up to 50% [5]. Diverse etiological factors such as fibrosis [6,7] and increased Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) activity [8,9] among others, are thought to play a key role in the initiation of oxidative AF [4,10]. While the causative and signaling factors of oxidative AF are reasonably well identified, the mechanism of spontaneous initiation (i.e., not induced by electrical stimulation) of acute oxidative AF in experimental and human studies, remains undefined [10].…”
Section: Introductionmentioning
confidence: 99%
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“…NADPH oxidases are major sources of reactive oxygen species, and activation of NADPH oxidases was associated with the incidence of AF 29, 30, 31, 32, 33, 34, 35, 36. Furthermore, several studies demonstrated that oxidative stress plays an important role in renal dysfunction–induced cardiac fibrosis, and AST‐120 prevented cardiac damage by alleviating oxidative stress 13, 15.…”
Section: Discussionmentioning
confidence: 99%