Population
Human patients with heart disease, as well as animal and cell models
Design
Review
Authors
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May inform arrhythmia substrate assessment; leaves open whether connexin43 modulation improves clinical outcomes.
Gap junction structural remodeling and altered connexin expression are key components of the pro-arrhythmic substrate in various forms of heart disease.
Nicholas J. Severs (2004) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: