ArticleJournal of the American Heart Association2024
Stroke Alters the Function of Enteric Neurons to Impair Smooth Muscle Relaxation and Dysregulates Gut Transit.
Article in Journal of the American Heart Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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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.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- European stroke organisation guideline on stroke-associated pneumonia.European stroke journal · 2026Guideline
- A roadmap towards clinical use of molecular biomarkers in acute ischaemic stroke.Nature reviews. Neurology · 2026Review
- Exploring the Mechanism of Medicated Thread Moxibustion of Zhuang Medicine in Diabetic Gastroparesis Rats Based on the Enteric Nervous System.Neurogastroenterology and motility · 2026Article
- Bone marrow-derived mesenchymal stem cells for ischemic stroke: mechanisms, delivery strategies, clinical evidence, and translational challenges.Stem cell research & therapy · 2026Review
- Amifostine alleviates ionizing radiation-induced small intestinal motility dysfunction in mice by remodeling the structure of the enteric nervous system.Histochemistry and cell biology · 2026Article
- Gut microbiome-immune-metabolic mechanisms in cerebrovascular disease: evidence-graded insights from cerebral small vessel disease, ischemic stroke, and intracerebral hemorrhage.Frontiers in microbiology · 2026Review
- Function of the large intestine and its interaction with the brain after ischemic stroke: a comprehensive literature review.Frontiers in cellular neuroscience · 2026Review
- Constipation in critically ill adults.World journal of gastrointestinal pathophysiology · 2025Review
- An ultrasonic degraded polysaccharide extracted from Pueraria lobata ameliorate ischemic brain injury in mice by regulating the gut microbiota and LPS-TLR4 pathway.Ultrasonics sonochemistry · 2025Article
- Assessing the impact of moxibustion on colonic mucosal integrity and gut microbiota in a rat model of cerebral ischemic stroke: insights from the "brain-gut axis" theory.Frontiers in neurology · 2025Article
- Systematic Insights into the Relationship between the Microbiota-Gut-Brain Axis and Stroke with the Focus on Tryptophan Metabolism.Metabolites · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGut dysmotility is common after ischemic stroke, but the mechanism underlying this response is unknown. Under homeostasis, gut motility is regulated by the neurons of the enteric nervous system that control contractile/relaxation activity of muscle cells in the gut wall. More recently, studies of gut inflammation revealed interactions of macrophages with enteric neurons are also involved in modulating gut motility. However, whether poststroke gut dysmotility is mediated by direct signaling to the enteric nervous system or indirectly via inflammatory macrophages is unknown. METHODS AND
resultsWe examined these hypotheses by using a clinically relevant permanent intraluminal midcerebral artery occlusion experimental model of stroke. At 24 hours after stroke, we performed in vivo and ex vivo gut motility assays, flow cytometry, immunofluorescence, and transcriptomic analysis. Stroke-induced gut dysmotility was associated with recruitment of muscularis macrophages into the gastrointestinal tract and redistribution of muscularis macrophages away from myenteric ganglia. The permanent intraluminal midcerebral artery occlusion model caused changes in gene expression in muscularis macrophages consistent with an altered phenotype. While the size of myenteric ganglia after stroke was not altered, myenteric neurons from post-permanent intraluminal midcerebral artery occlusion mice showed a reduction in neuronal nitric oxide synthase expression, and this response was associated with enhanced intestinal smooth muscle contraction ex vivo. Finally, chemical sympathectomy with 6-hydroxydopamine prevented the loss of myenteric neuronal nitric oxide synthase expression and stroke-induced slowed gut transit.
conclusionsOur findings demonstrate that activation of the sympathetic nervous system after stroke is associated with reduced neuronal nitric oxide synthase expression in myenteric neurons, resulting in impaired smooth muscle relaxation and dysregulation of gut transit.
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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 Socratic graph.