ArticleScientific reports2016
Sympathetic neurons are a powerful driver of myocyte function in cardiovascular disease.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- A reproducible and physiologically relevant human iPSC-derived platform for in vitro modeling of the neurocardiac junction.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Multimodal, device-based therapeutic targeting of the cardiovascular autonomic nervous system.Nature reviews. Cardiology · 2026Review
- Sympathetic-like-integrated engineered heart tissue models AGEs-induced adverse remodeling.Cardiovascular diabetology · 2026Article
- Electrophysiological comparison of left versus right stellate ganglia neurons.Journal of molecular and cellular cardiology plus · 2025Article
- Cardiac sympathetic neurons are additional cells affected in genetically determined arrhythmogenic cardiomyopathy.The Journal of physiology · 2025Article
- Molecular and cellular neurocardiology in heart disease.The Journal of physiology · 2025Review
- A modular platform to generate functional sympathetic neuron-innervated heart assembloids.Research square · 2024Article
- Exploring the prospects, advancements, and challenges ofFrontiers in cellular neuroscience · 2024Article
- Neurochemical alterations of intrinsic cardiac ganglionated nerve plexus caused by arterial hypertension developed during ageing in spontaneously hypertensive and Wistar Kyoto rats.Journal of anatomy · 2023Article
- Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
- Human induced pluripotent stem cell-derived cardiac myocytes and sympathetic neurons in disease modelling.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Article
- PC6 electroacupuncture reduces stress-induced autonomic and neuroendocrine responses in rats.Heliyon · 2023Article
- O-GlcNAcylation is crucial for sympathetic neuron development, maintenance, functionality and contributes to peripheral neuropathy.Frontiers in neuroscience · 2023Article
- Norepinephrine transporter defects lead to sympathetic hyperactivity in Familial Dysautonomia models.Nature communications · 2022Article
- Abnormal Cyclic Nucleotide Signaling at the Outer Mitochondrial Membrane In Sympathetic Neurons During the Early Stages of Hypertension.Hypertension (Dallas, Tex. : 1979) · 2022Article
- Nerve growth factor transfer from cardiomyocytes to innervating sympathetic neurons activates TrkA receptors at the neuro-cardiac junction.The Journal of physiology · 2022Article
- Healthy cardiac myocytes can decrease sympathetic hyperexcitability in the early stages of hypertension.Frontiers in synaptic neuroscience · 2022Article
- Heightened sympathetic neuron activity and altered cardiomyocyte properties in spontaneously hypertensive rats during the postnatal period.Frontiers in synaptic neuroscience · 2022Article
- From Mice to Mainframes: Experimental Models for Investigation of the Intracardiac Nervous System.Journal of cardiovascular development and disease · 2021Review
- Optical Interrogation of Sympathetic Neuronal Effects on Macroscopic Cardiomyocyte Network Dynamics.iScience · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Many therapeutic interventions in disease states of heightened cardiac sympathetic activity are targeted to the myocytes. However, emerging clinical data highlights a dominant role in disease progression by the neurons themselves. Here we describe a novel experimental model of the peripheral neuro-cardiac axis to study the neuron's ability to drive a myocyte cAMP phenotype. We employed a co-culture of neonatal ventricular myocytes and sympathetic stellate neurons from normal (WKY) and pro-hypertensive (SHR) rats that are sympathetically hyper-responsive and measured nicotine evoked cAMP responses in the myocytes using a fourth generation FRET cAMP sensor. We demonstrated the dominant role of neurons in driving the myocyte ß-adrenergic phenotype, where SHR cultures elicited heightened myocyte cAMP responses during neural activation. Moreover, cross-culturing healthy neurons onto diseased myocytes rescued the diseased cAMP response of the myocyte. Conversely, healthy myocytes developed a diseased cAMP response if diseased neurons were introduced. Our results provide evidence for a dominant role played by the neuron in driving the adrenergic phenotype seen in cardiovascular disease. We also highlight the potential of using healthy neurons to turn down the gain of neurotransmission, akin to a smart pre-synaptic ß-blocker.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.