Notwithstanding these important unresolved questions, the Zhu et al. ( 5) study should open up a new area of investigation as additional studies probe the connections between β 1 -adrenergic receptor-mediated signaling and CaMKII-dependent effects.If future studies support the proposal by Zhu et al., that one of the consequences of prolonged β 1 -adrenergic receptor stimulation is cardiomyocyte cell death via a CaMKII-mediated pathway, it will indeed be an important contribution to our understanding of the pathogenesis of heart failure that will suggest novel therapeutic targets.1.
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