Evidence map›Paper›PMID 36279071›Full record

ReviewTranslational stroke research2023

Gut Microbiota in Ischemic Stroke: Role of Gut Bacteria-Derived Metabolites.

Wei Zhang, Xiao Yu Dong, Rui Huang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Translational stroke research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. [Research progress on the mechanism and potential applications of gut microbiota-derived extracellular vesicles in ischemic stroke].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Gut microbes · 2025
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Decoding Blastocystis-Driven Mechanisms in Gut Microbiota and Host Metabolism.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  18. Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Wei ZhangDepartment of Neurology, Shengjing Hospital of China Medical University, Shenyang, China.
Xiao Yu DongDepartment of Neurology, Shengjing Hospital of China Medical University, Shenyang, China.
Rui HuangDepartment of Neurology, Shengjing Hospital of China Medical University, Shenyang, China. huangr_cmu@163.com.ORCID http://orcid.org/0000-0002-4254-4685
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke (IS) remains a leading cause of death and long-term disability globally. Several mechanisms including glutamate excitotoxicity, calcium overload, neuroinflammation, oxidative stress, mitochondrial damage, and apoptosis are known to be involved in the pathogenesis of IS, but the underlying pathophysiology mechanisms of IS are not fully clarified. During the past decade, gut microbiota were recognized as a key regulator to affect the health of the host either directly or via their metabolites. Recent studies indicate that gut bacterial dysbiosis is closely related to hypertension, diabetes, obesity, dyslipidemia, and metabolic syndrome, which are the main risk factors for cardiovascular diseases. Increasing evidence indicates that IS can lead to perturbation in gut microbiota and increased permeability of the gut mucosa, known as "leaky gut," resulting in endotoxemia and bacterial translocation. In turn, gut dysbiosis and impaired intestinal permeability can alter gut bacterial metabolite signaling profile from the gut to the brain. Microbiota-derived products and metabolites, such as short-chain fatty acids (SCFAs), bile acids (BAs), trimethylamine N-oxide (TMAO), lipopolysaccharides (LPS), and phenylacetylglutamine (PAGln) can exert beneficial or detrimental effects on various extraintestinal organs, including the brain, liver, and heart. These metabolites have been increasingly acknowledged as biomarkers and mediators of IS. However, the specific role of the gut bacterial metabolites in the context of stroke remains incompletely understood. In-depth studies on these products and metabolites may provide new insight for the development of novel therapeutics for IS.

Indexed as

Gastrointestinal MicrobiomeIschemic StrokeStrokeBacteriaDysbiosisHumansBile acidsIschemic strokeLipopolysaccharidesPhenylacetylglutamineShort-chain fatty acidsTrimethylamine N-oxide

Identifiers

PMID36279071
OpenAlexW4307134671

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.