Low‐Affinity Nerve Growth Factor Receptor p75NTR Immunoreactivity in the Myocardium with Sympathetic Hyperinnervation
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Summary
The aim of this study was to determine the density and location of TrkA and p75NTR in canine ventricles with sympathetic hyperinnervation and to investigate the relationship between sympathetic nerve density in myocardium and the occurrences of ventricular arrhythmia.
- Type
- article
- Published
- 2004-04-01
- Cited by
- 13
- References
- 33
- OpenAlex
- https://openalex.org/W15089992
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:19153564
Keywords
Geography
References
- Cellular localization of the Trk neurotrophin receptor family in human non-neuronal tissues.
- Complete ablation of the neurotrophin receptor p75NTR causes defects both in the nervous and the vascular system
- The neurotrophic factor concept: a reexamination
- p75 Is Important for Axon Growth and Schwann Cell Migration during Development
- Nerve sprouting and sudden cardiac death.
- Overexpression of NGF within the heart of transgenic mice causes hyperinnervation, cardiac enlargement, and hyperplasia of ectopic cells.
- Activation of the sphingomyelin cycle through the low-affinity neurotrophin receptor.
- c-fos protooncogene expression in rat hippocampus and entorhinal cortex following tetanic stimulation of the perforant path.
- Nerve growth factor derived from terminals selectively increases the ratio of p75 to trkA NGF receptors on mature sympathetic neurons.
- Nerve Sprouting and Sympathetic Hyperinnervation in a Canine Model of Atrial Fibrillation Produced by Prolonged Right Atrial Pacing
- Nerve growth factor in sympathetic ganglia and corresponding target organs of the rat: correlation with density of sympathetic innervation.
- Superinduction of c-fos by nerve growth factor in the presence of peripherally active benzodiazepines.
- Sympathetic and sensory axons invade the brains of nerve growth factor transgenic mice in the absence of p75NTR expression.
- Atrial fibrillation produced by prolonged rapid atrial pacing is associated with heterogeneous changes in atrial sympathetic innervation.
- Death of oligodendrocytes mediated by the interaction of nerve growth factor with its receptor p75
- Nerve growth factor and its low-affinity receptor promote Schwann cell migration.
- Long-term subthreshold electrical stimulation of the left stellate ganglion and a canine model of sudden cardiac death.
- Nerve growth factor-induced growth of sympathetic axons into the optic tract of mature mice is enhanced by an absence of p75NTR expression.
- Developmental changes of nerve growth factor levels in sympathetic ganglia and their target organs.
- Synaptic reorganization in the hippocampus induced by abnormal functional activity.
Cited by
- P75 neurotrophin receptor is a regulatory factor in sudden cardiac death with myocardial infarction.
- Clearer Connections:
- Regulation of pro-inflammatory and pro-fibrotic factors by CCN2/CTGF in H9c2 cardiomyocytes
- Evidence for Increased Atrial Sympathetic Innervation in Persistent Human Atrial Fibrillation
- Heterogeneous ventricular sympathetic innervation, altered beta-adrenergic receptor expression, and rhythm instability in mice lacking the p75 neurotrophin receptor.
- Spontaneous Atrial Fibrillation Initiated by Tyramine in Canine Atria with Increased Sympathetic Nerve Sprouting
- Dexmedetomidine for the treatment of paroxysmal autonomic instability with dystonia
- The p75 neurotrophin receptor, semaphorins, and sympathetic traffic in the heart.
- A novel peptide ghrelin inhibits neural remodeling after myocardial infarction in rats.
- Neurotrophic Factors and Heart Diseases
- p75 neurotrophin receptor modulates the development and post-infarct remodeling of cardiac sympathetic neurons
- Cardiac autonomic denervation and expression of neurotrophins (NGF and BDNF) and their receptors during experimental Chagas disease
- AP-1 Is Required For CMX-8933-Induced SOD Upregulation And Is Translocated In Response To A Human EPN Mimetic
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