Key result
Selective chemogenetic activation of intracardiac cholinergic neurons lessens cardiac dysfunction and mortality in a rat model of pressure overload-induced heart failure.
Why the study?
Does chemogenetic activation of intracardiac cholinergic neurons improve cardiac function and reduce mortality in a rat model of pressure overload-induced heart failure?
Does chemogenetic activation of intracardiac cholinergic neurons improve cardiac function and reduce mortality in a rat model of pressure overload-induced heart failure?
Chemogenetic activation of intracardiac cholinergic neurons represents a novel, cardiac-selective target for increasing cardioprotective parasympathetic activity and reducing mortality in heart failure.
Should not alter HF management; leaves open translation of intracardiac cholinergic activation to larger models.
Intracardiac ganglia form the final common pathway for the parasympathetic innervation of the heart. This study has used a novel chemogenetic approach within transgenic ChAT-Cre rats [expressing only Cre-recombinase in choline acetyl transferase (ChAT) neurons] to selectively increase intracardiac cholinergic parasympathetic activity to the heart in a pressure overload-induced heart failure model. The findings from this study confirm that selective activation of intracardiac cholinergic neurons lessens cardiac dysfunction and mortality seen in heart failure, identifying a novel downstream cardiac-selective target for increasing cardioprotective parasympathetic activity in heart failure.
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Dyavanapalli et al. (2020) studied Pressure overload-induced heart failure. Chemogenetic activation of intracardiac cholinergic neurons was evaluated on Cardiac dysfunction and mortality. Selective chemogenetic activation of intracardiac cholinergic neurons lessens cardiac dysfunction and mortality in a rat model of pressure overload-induced heart failure.
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