Redox State in Atrial Fibrillation Pathogenesis and Relevant Therapeutic Approaches
-
Published:2019-04-22
Issue:5
Volume:26
Page:765-779
-
ISSN:0929-8673
-
Container-title:Current Medicinal Chemistry
-
language:en
-
Short-container-title:CMC
Author:
Antonopoulos Alexios S.1, Goliopoulou Athina1, Oikonomou Evangelos1, Tsalamandris Sotiris1, Papamikroulis Georgios-Angelos1, Lazaros George1, Tsiamis Eleftherios1, Latsios George1, Brili Stella1, Papaioannou Spyridon1, Gennimata Vasiliki1, Tousoulis Dimitris1
Affiliation:
1. 1st Cardiology Department, Athens Medical School, Athens, Greece
Abstract
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 redoxtargeting
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.
Publisher
Bentham Science Publishers Ltd.
Subject
Pharmacology,Molecular Medicine,Drug Discovery,Biochemistry,Organic Chemistry
Reference110 articles.
1. Bonilla IM, Sridhar A, Györke S, Cardounel AJ, Carnes CA. Nitric oxide synthases and atrial fibrillation. 2. Reilly SN, Liu X, Carnicer R, Recalde A, Muszkiewicz A, Jayaram R, Carena MC, Wijesurendra R, Stefanini M, Surdo NC, Lomas O, Ratnatunga C, Sayeed R, Krasopoulos G, Rajakumar T, Bueno-Orovio A, Verheule S, Fulga TA, Rodriguez B, Schotten U, Casadei B. Up-regulation of miR-31 in human atrial fibrillation begets the arrhythmia by depleting dystrophin and neuronal nitric oxide synthase. 3. Simon JN, Ziberna K, Casadei B. Compromised redox homeostasis, altered nitroso-redox balance, and therapeutic possibilities in atrial fibrillation. 4. Antoniades C, Antonopoulos AS, Bendall JK, Channon KM. Targeting redox signaling in the vascular wall: From basic science to clinical practice. 5. Antoniades C, Demosthenous M, Reilly S, Margaritis M, Zhang MH, Antonopoulos A, Marinou K, Nahar K, Jayaram R, Tousoulis D, Bakogiannis C, Sayeed R, Triantafyllou C, Koumallos N, Psarros C, Miliou A, Stefanadis C, Channon KM, Casadei B. Myocardial redox state predicts in-hospital clinical outcome after cardiac surgery effects of short-term pre-operative statin treatment.
Cited by
11 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献
|
|