Genetically engineered murine models and in vivo electrophysiology study techniques provide important insights into the molecular mechanisms underlying cardiac conduction and arrhythmogenesis.
This review summarizes current in vivo electrophysiology techniques and genetic mouse models used to study human arrhythmia disorders.
Advances in transgene and gene targeting technology have enabled sophisticated manipulation of the mouse genome, providing important insights into the molecular mechanisms underlying cardiac conduction, arrhythmogenesis, and sudden cardiac death. The mouse is currently the principal mammalian model for studying biological processes, particularly related to cardiac pathophysiology. Murine models have been engineered harboring gene mutations leading to inherited structural and electrical disorders of the heart due to transcription factor mutations, connexin protein defects, and G protein and ion channelopathies. These mutations lead to phenotypes reminiscent of human clinical disease states including congenital heart defects, cardiomyopathies, and long-QT syndrome, creating models of human electrophysiological disease. Functional analyses of the underlying molecular mechanisms of resultant phenotypes require appropriate and sophisticated experimental methodology. This paper reviews current in vivo murine electrophysiology study techniques and genetic mouse models pertinent to human arrhythmia disorders.
Charles I. Berul (Tue,) conducted a review in Cardiac pathophysiology and arrhythmia disorders. In vivo murine electrophysiology study techniques and genetic mouse models was evaluated. Genetically engineered murine models and in vivo electrophysiology study techniques provide important insights into the molecular mechanisms underlying cardiac conduction and arrhythmogenesis.
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