Evidence map›Paper›PMID 38030854›Full record

ArticleTranslational stroke research2025

Sympathetic-Mediated Intestinal Cell Death Contributes to Gut Barrier Impairment After Stroke.

Kathryn Prame Kumar, Liam D McKay, Huynh Nguyen, Jasveena Kaur, Jenny L Wilson, Althea R Suthya, Sonja J McKeown, Helen E Abud, Connie H Y Wong

Open access · hybridAbstract read
In one paragraph

Article in Translational stroke research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 13 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Kathryn Prame Kumar *Centre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences at Monash Health, Monash Medical Centre, Monash University, Clayton, VIC, 3168, Australia.
Liam D McKay *Centre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences at Monash Health, Monash Medical Centre, Monash University, Clayton, VIC, 3168, Australia.
Huynh NguyenCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences at Monash Health, Monash Medical Centre, Monash University, Clayton, VIC, 3168, Australia.
Jasveena KaurDepartment of Anatomy and Developmental Biology, Development and Stem Cells Program, Biomedical Discovery Institute, Monash University, Clayton, VIC, 3800, Australia.
Jenny L WilsonCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences at Monash Health, Monash Medical Centre, Monash University, Clayton, VIC, 3168, Australia.
Althea R SuthyaCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences at Monash Health, Monash Medical Centre, Monash University, Clayton, VIC, 3168, Australia.
Sonja J McKeownDepartment of Anatomy and Developmental Biology, Development and Stem Cells Program, Biomedical Discovery Institute, Monash University, Clayton, VIC, 3800, Australia.
Helen E AbudDepartment of Anatomy and Developmental Biology, Development and Stem Cells Program, Biomedical Discovery Institute, Monash University, Clayton, VIC, 3800, Australia.
Connie H Y WongCentre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences at Monash Health, Monash Medical Centre, Monash University, Clayton, VIC, 3168, Australia. connie.wong@monash.edu.
Monash University · AUMonash Health · AUMonash Medical Centre · AU

Funding

CSL Limited WongNational Health and Medical Research Council GNT1184517National Heart Foundation of Australia 102796
6 · The paper itself

Abstract

Tissue injury induced by stroke is traditionally thought to be localised to the brain. However, there is an accumulating body of evidence to demonstrate that stroke promotes pathophysiological consequences in peripheral tissues including the gastrointestinal system. In this study, we investigated the mechanisms underlying gut permeability after stroke. We utilised the clinically relevant experimental model of stroke called permanent intraluminal middle cerebral artery occlusion (pMCAO) to examine the effect of cerebral ischaemia on the gut. We detected stroke-induced gut permeability at 5 h after pMCAO. At this timepoint, we observed significantly elevated intestinal epithelial cell death in post-stroke mice compared to their sham-operated counterparts. At 24 h after stroke onset when the gut barrier integrity is restored, our findings indicated that post-stroke intestinal epithelium had higher expression of genes associated with fructose metabolism, and hyperplasia of intestinal crypts and goblet cells, conceivably as a host compensatory mechanism to adapt to the impaired gut barrier. Furthermore, we discovered that stroke-induced gut permeability was mediated by the activation of the sympathetic nervous system as pharmacological denervation decreased the stroke-induced intestinal epithelial cell death, goblet cell and crypt hyperplasia, and gut permeability to baseline levels. Our study identifies a previously unknown mechanism in the brain-gut axis by which stroke triggers intestinal cell death and gut permeability.

Indexed as

Cell DeathIntestinal MucosaStrokeSympathetic Nervous SystemAnimalsDisease Models, AnimalInfarction, Middle Cerebral ArteryMaleMiceMice, Inbred C57BLPermeabilityBarrier integrityBrain-gut axisCerebral ischaemiaEpitheliumGut permeability

Identifiers

PMID38030854
PMCPMC11976816
OpenAlexW4389153198

What OpenQuestion holds

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Registered trials

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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.