2007
DOI: 10.1016/s0828-282x(07)71006-1
|View full text |Cite
|
Sign up to set email alerts
|

Ischemic, genetic and pharmacological origins of cardiac arrhythmias: The contribution of the Quebec Heart Institute

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
4
0
2

Year Published

2014
2014
2022
2022

Publication Types

Select...
5

Relationship

0
5

Authors

Journals

citations
Cited by 5 publications
(6 citation statements)
references
References 85 publications
0
4
0
2
Order By: Relevance
“…The augmented systemic oxidative stress is associated with cardiac electrical and structural remodelling [ 26 28 ], and reactive oxygen species may impair Na, K, Ca channels and Na-Ca exchanger activity, leading to gap junction remodelling, decreasing the action potential amplitude and duration, and increasing the incidence of cardiac arrhythmias in animal models [ 15 ]. In fact, oxidative stress results in decreased hERG protein levels, accelerated activation and deactivation of hERG, increased in current amplitude of hERG and hKv1.5, allowing a greater amount of K ions to flow through these channels in the phase 3 of the action potential, down regulation of Ito (transient outward potassium current) responsible for the rapid repolarization phase, and increased the channel opening probability of Ik1 (inward rectifying channel) [ 27 , 28 ].…”
Section: Resultsmentioning
confidence: 99%
“…The augmented systemic oxidative stress is associated with cardiac electrical and structural remodelling [ 26 28 ], and reactive oxygen species may impair Na, K, Ca channels and Na-Ca exchanger activity, leading to gap junction remodelling, decreasing the action potential amplitude and duration, and increasing the incidence of cardiac arrhythmias in animal models [ 15 ]. In fact, oxidative stress results in decreased hERG protein levels, accelerated activation and deactivation of hERG, increased in current amplitude of hERG and hKv1.5, allowing a greater amount of K ions to flow through these channels in the phase 3 of the action potential, down regulation of Ito (transient outward potassium current) responsible for the rapid repolarization phase, and increased the channel opening probability of Ik1 (inward rectifying channel) [ 27 , 28 ].…”
Section: Resultsmentioning
confidence: 99%
“…Obese subjects exhibit increased systemic oxidative stress, enhanced by abdominal adiposity and associated with adiponectin deficiency [135]. Recent clinical and experimental evidence demonstrated the involvement of oxidative stress in cardiac electrical and structural remodeling [23,136,137]. Reactive oxygen species may impair Na, K and Ca channels, Na-Ca exchanger activity, may be implicated in gap junction remodeling, decrease the action potential amplitude and duration, and increase the incidence of cardiac arrhythmias in animal models [136][137][138][139][140].…”
Section: Oxidative Stress and Arrhythmogenesismentioning
confidence: 99%
“…Oxidative stress results in decreased hERG protein levels, accelerated activation and deactivation of hERG, and increase in current amplitude of hERG and hKv1.5, allowing a greater amount of K ions to flow through these channels in the phase 3 of the action potential, downregulation of Ito (responsible for the rapid repolarization phase), and increases the channel opening probability of Ik1 (inward rectifying channel) [136,137].…”
Section: Oxidative Stress and Arrhythmogenesismentioning
confidence: 99%
“…The AGEs/RAGE axis can elicit mitochondrial dysfunction and generate reactive oxygen species (ROS), which in turn activate a nuclear factor kappa B (NFκB) cascade (Gloire et al, 2006 ; Wang et al, 2015 ; Wautier et al, 2001 ; Yamagishi et al, 2015 ). Augmented systemic oxidative stress is associated with cardiac electrical and structural remodeling, which may impair Na + , potassium (K + ), and calcium (Ca 2+ ) channels and Na–Ca exchanger (NCX) activity, thus leading to gap junction remodeling, decreased action potential (AP) amplitude (APA) and AP duration (APD), and increased incidence of cardiac arrhythmia in animal models (Dong & Ren, 2014 ; Drolet et al, 2007 ; Jeong et al, 2012 ).…”
Section: Introductionmentioning
confidence: 99%