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Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
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Connexin Remodeling Contributes to Atrial Fibrillation
Michelle M Jennings1, J Kevin Donahue1
1Case Western Reserve University School of Medicine, MetroHealth Campus.
Journal of Atrial Fibrillation
|May 13, 2017
Summary
Atrial fibrillation involves changes in gap junction proteins, connexins 40 and 43. This remodeling creates electrical instability, promoting sustained reentry and atrial fibrillation.
Area of Science:
- Cardiology
- Electrophysiology
- Molecular Biology
Background:
- Atrial fibrillation (AF) is a major cause of stroke, heart failure, and myocardial infarction.
- Gap junctional remodeling, particularly involving connexins 40 and 43, is crucial in AF development and maintenance.
- Altered connexin expression and localization create a substrate for sustained reentry in AF.
Purpose of the Study:
- To review the mechanisms of atrial fibrillation (AF) related to connexin remodeling.
- To discuss the role of connexins 40 and 43 in AF pathogenesis.
- To explore connexin remodeling as a potential therapeutic target for AF.
Main Methods:
- Literature review of studies investigating atrial fibrillation mechanisms.
- Analysis of research on connexin expression and localization in AF.
- Synthesis of information on the role of gap junctions in cardiac electrical activity.
Main Results:
- Connexin 40 and 43 undergo significant alterations in atrial fibrillation.
- These connexin changes promote an environment conducive to sustained reentry.
- The reentrant substrate is key for AF initiation and maintenance.
Conclusions:
- Connexin remodeling is a fundamental mechanism underlying atrial fibrillation.
- Targeting connexin alterations may offer novel therapeutic strategies for AF.
- Further research into connexin function in AF is warranted.
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