TY - JOUR
TI - Redox State in Atrial Fibrillation Pathogenesis and Relevant Therapeutic
Approaches
AU - Antonopoulos, Alexios S.
AU - Goliopoulou, Athina
AU - Oikonomou,
AU - Evangelos
AU - Tsalamandris, Sotiris
AU - Papamikroulis, Georgios-Angelos
AU - and Lazaros, George
AU - Tsiamis, Eleftherios
AU - Latsios, George and
AU - Brili, Stella
AU - Papaioannou, Spyridon
AU - Gennimata, Vasiliki and
AU - Tousoulis, Dimitris
JO - Current Medicinal Chemistry
PY - 2019
VL - 26
TODO - 5
SP - 765-779
PB - BENTHAM SCIENCE PUBL LTD
SN - 0929-8673
TODO - 10.2174/0929867324666170718130408
TODO - Myocardial redox; oxidative stress; superoxide; NADPH; nitric oxide;
atrial fibrillation
TODO - Background: Myocardial redox state is a critical determinant of atrial
biology, regulating cardiomyocyte apoptosis, ion channel function, and
cardiac hypertrophy/fibrosis and function. Nevertheless, it remains
unclear whether the targeting of atrial redox state is a rational
therapeutic strategy for atrial fibrillation prevention.
Objective: To review the role of atrial redox state and anti-oxidant
therapies in atrial fibrillation.
Method: Published literature in Medline was searched for experimental
and clinical evidence linking myocardial redox state with atrial
fibrillation pathogenesis as well as studies looking into the role of
redox-targeting therapies in the prevention of atrial fibrillation.
Results: Data from animal models have shown that altered myocardial
nitroso-redox balance and NADPH oxidases activity are causally involved
in the pathogenesis of atrial fibrillation. Similarly experimental
animal data supports that increased reactive oxygen/nitrogen species
formation in the atrial tissue is associated with altered
electrophysiological properties of atrial myocytes and electrical
remodeling, favoring atrial fibrillation development. In humans,
randomized clinical studies using redox-related therapeutic approaches
(e.g. statins or antioxidant agents) have not documented any benefits in
the prevention of atrial fibrillation development (mainly post-operative
atrial fibrillation risk).
Conclusion: Despite strong experimental and translational data
supporting the role of atrial redox state in atrial fibrillation
pathogenesis, such mechanistic evidence has not been translated to
clinical benefits in atrial fibrillation risk in randomized clinical
studies using redox-related therapies.
ER -