Dilated cardiomyopathy remodels cardiac neuronal subtypes in a murine model

The autonomic nervous system is comprised of two parallel chains sympathetic and parasympathetic nervous system that innervates myocardium heterogeneously. However, excessive sympathetic signalling is a hallmark of cardiac dysfunction including myocardial infarction and cardiomyopathies. In current research article, first, we carried out echocardiography on DCM-Tg9 mice to characterize cardiac output parameters and performed scRNAseq analysis in a dilated cardiomyopathy mouse model of heart-failure over wildtype control mice. We analysed differential gene expressions and performed pathway enrichment analysis. The important findings of our research indicate the increment within a specific neuronal subpopulation (NA1b) out of three adrenergic cardiac innervating neuronal subpopulation. We also observed significant increase in M-current potassium ion channel (Kcnq2 ion channel) and genes involved in pathways from oxidative phosphorylation and neurodegeneration pathways. These observations have clearly interpreted that significantly elevated expression of M-current ion channels might be involved with hyperactivated sympathetic signalling in heart-failure mice. HighlightsO_LIWe identified three adrenergic neuronal subtypes that innervate myocardium and one of these neuronal subtypes, NA1b, predominantly presents during the heart-failure. C_LIO_LIOur results indicated presence of m-current ion channels (Kcnq2) significantly elevated during heart failure in a murine dilated cardiomyopathy model. C_LIO_LIThe pathway enrichment analyses showed increased expression of genes that are involved in neurodegenerative and oxidative pathways. C_LI