ArticleJCI insight2017
Inflammation, oxidative stress, and glial cell activation characterize stellate ganglia from humans with electrical storm.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 103 citations in OpenAlex.
- Effect of ultrasound-guided stellate ganglion block on inflammatory cytokines and postoperative recovery after partial hepatectomy: a randomised clinical trial.BMC anesthesiology · 2024Trial
- Three-Dimensional Magnetic Resonance Imaging of the Human Stellate Ganglion.Clinical anatomy (New York, N.Y.) · 2026Review
- Stellate Ganglion Nrf2 Modulates Oxidative Stress and Heart Rate Responses in Mice and Rats with Heart Failure.Antioxidants (Basel, Switzerland) · 2026Article
- Systemic Neutralization of Granulocyte-Macrophage Colony-Stimulating Factor Attenuates Stellate Ganglion Neuroinflammation and Cardiac Sympathetic Overactivation in Chronic Heart Failure in Rats.International journal of molecular sciences · 2026Article
- Spinal nociceptive denervation impedes subsequent chronic autonomic remodeling after myocardial infarction in male swine.Nature communications · 2026Article
- Article
- Noradrenergic and cholinergic innervation of the normal human heart and changes associated with cardiomyopathy.Anatomical record (Hoboken, N.J. : 2007) · 2026Article
- Glial cells in the heart: Implications for their roles in health and disease.The Journal of physiology · 2026Review
- Impact of PKC-MAPK Signaling on Cardiac Sympathetic Overactivation in Type-2 Diabetes Mellitus.International journal of molecular sciences · 2026Article
- The neuroimmune axis in cardiovascular disease: from immune activation to inflammatory resolution.Frontiers in immunology · 2026Review
- Glia of the heart's nervous system.Nature reviews. Neuroscience · 2025Review
- Anatomy, Imaging, and Clinical Significance of the Cervicothoracic (Stellate) Ganglion.Diagnostics (Basel, Switzerland) · 2025Review
- Autonomic Imbalance in Cardiomyopathy and Heart Failure: From Neurobiology to Precision Neuromodulation.Current cardiology reports · 2025Review
- Review
- Mind the GAPS: Glia associated with psychological stress.Journal of neuroendocrinology · 2025Review
- Ventricular Arrhythmias and Myocardial Infarction: Electrophysiological and Neuroimmune Mechanisms.Biomedicines · 2025Review
- Stellate Ganglia: A Key Therapeutic Target for Malignant Ventricular Arrhythmia in Heart Disease.Circulation research · 2025Review
- Renal denervation achieves its antiarrhythmic effect through attenuating macrophage activation and neuroinflammation in stellate ganglia in chronic heart failure.Cardiovascular research · 2025Article
- Age-dependent reduction in voltage-gated inward sodium current and Scn8a gene expression in murine stellate ganglia.Annals of the New York Academy of Sciences · 2025Article
- Bayliss Starling Prize Lecture 2023: Neuropeptide-Y being 'unsympathetic' to the broken hearted.The Journal of physiology · 2025Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundNeuronal remodeling in human heart disease is not well understood.
methodsStellate ganglia from patients with cardiomyopathy (CMY) and refractory ventricular arrhythmias undergoing cardiac sympathetic denervation (n = 8), and from organ donors with normal hearts (n = 8) collected at the time of organ procurement were compared. Clinical data on all subjects were reviewed. Electron microscopy (EM), histologic, and immunohistochemical assessments of neurotransmitter profiles, glial activation and distribution, and lipofuscin deposition, a marker of oxidative stress, were quantified.
resultsIn CMY specimens, lipofuscin deposits were larger, and present in more neurons (26.3% ± 6.3% vs. 16.7% ± 7.6%, P < 0.043), than age-matched controls. EM analysis revealed extensive mitochondrial degeneration in CMY specimens. T cell (CD3+) infiltration was identified in 60% of the CMY samples, with one case having large inflammatory nodules, while none were identified in controls. Myeloperoxidase-immunoreactive neutrophils were also identified at parenchymal sites distinct from inflammatory foci in CMY ganglia, but not in controls. The adrenergic phenotype of pathologic samples revealed a decrease in tyrosine hydroxylase staining intensity compared with controls. Evaluation of cholinergic phenotype by staining for the vesicular acetylcholine transporter revealed a low but comparable number of cholinergic neurons in ganglia from both groups and demonstrated that preganglionic cholinergic innervation was maintained in CMY ganglia. S100 staining (a glial cell marker) demonstrated no differences in glial distribution and relationship to neurons; however, glial activation demonstrated by glial fibrillary acidic protein (GFAP) staining was substantially increased in pathologic specimens compared with controls.
conclusionsStellate ganglia from patients with CMY and arrhythmias demonstrate inflammation, neurochemical remodeling, oxidative stress, and satellite glial cell activation. These changes likely contribute to excessive and dysfunctional efferent sympathetic tone, and provide a rationale for sympathectomy as a treatment for arrhythmias in this population.
fundingThis work was made possible by support from NIH grants HL125730 to OAA, GM107949 to DBH, and HL084261 and OT2OD023848 to KS.
Indexed as
Identifiers
What OpenQuestion holds
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.