Key result
Perinatal loss of Nkx2-5 in neonatal mice resulted in rapid conduction and contraction defects, accompanied by reduced ventricular expression of Na(v)1.5-alpha and ryanodine receptor 2.
Population
Tamoxifen-inducible Nkx2-5 knockout mice (neonates)
Design
Preclinical
Follow-up
4 days
Authors
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Nkx2-5 loss may impair neonatal conduction; hypothesis-generating for human arrhythmias and requires clinical validation.
Nkx2-5 is critical not only during early embryonic cardiac development but also in perinatal hearts for regulating genes involved in conduction and contraction.
Briggs et al. (2008) studied Conduction and contraction defects. Perinatal loss of Nkx2-5 via tamoxifen-inducible knockout was evaluated on Conduction and contraction, expression of Na(v)1.5-alpha and ryanodine receptor 2. Perinatal loss of Nkx2-5 in neonatal mice resulted in rapid conduction and contraction defects, accompanied by reduced ventricular expression of Na(v)1.5-alpha and ryanodine receptor 2.
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