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An Invited Review following the Soujinkai Young Investigator Award: Modulating Calmodulin-Ryanodine Receptor Binding as a Strategy to Halt Pressure-Overload Induced Cardiac Hypertrophy
Full text linkCardiac hypertrophy is widely recognized as a significant risk factor contributing to adverse outcomes in individuals with cardiovascular conditions. The disruption of intracellular calcium ( Ca^{2+} ) balance has been implicated in the development of cardiac hypertrophy, though the precise mechanisms remain poorly understood. In this research, we explored whether hypertrophy induced by pressure overload may arise from the destabilization of the cardiac ryanodine receptor (RyR2) triggered by the dissociation of calmodulin (CaM), leading to subsequent Ca^{2+} leakage. We also assessed whether genetically strengthening the binding affinity between CaM and RyR2 could potentially reverse this process. In the early phases of cardiac hypertrophy caused by pressure overload—when contractile function is still intact—we observed that RyR2 destabilization mediated by reactive oxygen species (ROS) coincides with impaired relaxation. Moreover, stabilizing RyR2 through enhanced CaM binding was found to completely inhibit hypertrophic signaling and improve survival rates. Our findings reveal a crucial connection between RyR2 destabilization and the progression of cardiac hypertrophy
Effects of Nodal Receptor Inhibition during Embryonic Stages of Development in Two Temnopleurid Sea Urchins
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Thioredoxin-interacting proteinは褐色脂肪組織の機能および急性寒冷ストレスへの適応的熱産生特性における重要な因子である
Full text link博士(医学)山口大学Yamaguchi Universit