Abnormal Conduction and Morphology in the Atrioventricular Node of Mice With Atrioventricular Canal–Targeted Deletion of Alk3/Bmpr1a Receptor
Author(s) -
Dina Myers Stroud,
Vinciane Gaussin,
John B.E. Burch,
Cindy Yu,
Yuji Mishina,
Michael Schneider,
Glenn I. Fishman,
Gregory E. Morley
Publication year - 2007
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.107.696583
Subject(s) - atrioventricular canal , medicine , bone morphogenetic protein , atrioventricular node , electrical conduction system of the heart , anatomy , sinoatrial node , cardiology , microbiology and biotechnology , biology , heart disease , electrocardiography , tachycardia , gene , genetics , heart rate , blood pressure
The atrioventricular (AV) node is essential for the sequential excitation and optimized contraction of the adult multichambered heart; however, relatively little is known about its formation from the embryonic AV canal. A recent study demonstrated that signaling by Alk3, the type 1a receptor for bone morphogenetic proteins, in the myocardium of the AV canal was required for the development of both the AV valves and annulus fibrosus. To test the hypothesis that bone morphogenetic protein signaling also plays a role in AV node formation, we investigated conduction system function and AV node morphology in adult mice with conditional deletion of Alk3 in the AV canal.
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