Oxidative stress in atrial fibrillation: An emerging role of NADPH oxidase

Abstract

Atrial fibrillation (AF) is the most common cardiac arrhythmia. Patients with AF have up to seven-fold higher risk of suffering from ischemic stroke. Better understanding of etiologies of AF and its thromboembolic complications are required for improved patient care, as current anti-arrhythmic therapies have limited efficacy and off target effects. Accumulating evidence has implicated a potential role of oxidative stress in the pathogenesis of AF. Excessive production of reactive oxygen species (ROS) is likely involved in the structural and electrical remodeling of the heart, contributing to fibrosis and thrombosis. In particular, NADPH oxidase (NOX) has emerged as a potential enzymatic source for ROS production in AF based on growing evidence from clinical and animal studies. Indeed, NOX can be activated by known upstream triggers of AF such as angiotensin II and atrial stretch. In addition, treatments such as Statins, antioxidants, ACEI or AT1RB have been shown to prevent post-operative AF; among which ACEI/AT1RB and Statins can attenuate NOX activity. On the other hand, detailed molecular mechanisms by which specific NOX isoform(s) are involved in the pathogenesis of AF and the extent to which activation of NOX plays a causal role in AF development remains to be determined. The current review discusses causes and consequences of oxidative stress in AF with a special focus on the emerging role of NOX pathways.

Extravirgin Olive Oil Consumption Reduces Risk of Atrial Fibrillation

“…[32][33][34][35][36][37] Moreover, a previous analysis of the PREDIMED trial found a significant reduction in C-reactive protein among participants assigned to the MeDiet+EVOO group but not in those assigned to the MeDiet+nuts group.…”

Selective downregulation of mitochondrial electron transport chain activity and increased oxidative stress in human atrial fibrillation

“…Moreover, it is not clear whether reported changes in myocardial energetics and mitochondrial function (1, 27, 56) are causative or the consequence of AF or associated conditions; nor is it clear whether the OXPHOS impairment reported in some (32) but not all (5a) animal studies also occurs in the human atria (12,37,50). Increasing evidence has accumulated that oxidative stress plays an important role in the pathogenesis of AF (47,17,62) and elevated oxidative stress markers are present in patients with AF (34,41,43,51). Oxidative stress can result from mitochondrial dysfunction with impairment in electron transport chain (ETC) activity (17), but this has not been systematically assessed in human atria.…”

A Role of Superoxide Dismutase in Development of Post-Operation Atrial Fibrillation in Coronary Heart Disease Patients

“…Значимые структурные изменения сердца, сопровождающиеся повышением окислительного стресса, могут быть объяснены увеличением внутри-клеточного содержания кальция, повышением уровня митохондриальных каспаз, ухудшением меж-клеточных щелевых контактов и сокращением реф-рактерного периода кардиомиоцитов [4,5]. Повыше-ние в послеоперационном периоде таких показате-лей, как ксантиноксидаза, транскрипционный фактор NF-κB и никотинамид-аденин-динуклео-тидфосфат оксидаза, по данным ряда авторов, также обуславливает развитие ПОФП [6,7]. В то же время, несмотря на большую роль супероксиддисмутазы (СОД) в развитии окислительного стресса, значение данного биомаркера в развитии ПОФП окончательно не установлено и требует дальнейшего изучения.…”