Evidence map›Paper›PMID 34421655›Full record

ArticleFrontiers in physiology2021

Intestinal Barrier Dysfunction Exacerbates Neuroinflammation via the TLR4 Pathway in Mice With Heart Failure.

Jun-Yu Huo, Wan-Ying Jiang, Ting Yin, Hai Xu, Yi-Ting Lyu, Yuan-Yuan Chen, Meng Chen, Jie Geng, Zhi-Xin Jiang, Qi-Jun Shan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

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  18. Selenium Nanoparticles-EnrichedInternational journal of nanomedicine · 2022
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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

10 authors at 2 institutions in 1 country.

Jun-Yu HuoDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wan-Ying JiangDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Ting YinDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Hai XuDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yi-Ting LyuDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yuan-Yuan ChenDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Meng ChenDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jie GengDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhi-Xin JiangDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Qi-Jun ShanDepartment of Cardiology, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jiangsu Province Hospital · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe present study aimed to investigate alterations in neuroinflammation after heart failure (HF) and explore the potential mechanisms.

methodsMale wild-type (WT) and Toll-like receptor 4 (TLR4)-knockout (KO) mice were subjected to sham operation or ligation of the left anterior descending coronary artery to induce HF. 8 weeks later, cardiac functions were analyzed by echocardiography, and intestinal barrier functions were examined by measuring tight junction protein expression, intestinal permeability and plasma metabolite levels. Alterations in neuroinflammation in the brain were examined by measuring microglial activation, inflammatory cytokine levels and the proinflammatory signaling pathway. The intestinal barrier protector intestinal alkaline phosphatase (IAP) and intestinal homeostasis inhibitor L-phenylalanine (L-Phe) were used to examine the relationship between intestinal barrier dysfunction and neuroinflammation in mice with HF.

resultsEight weeks later, WT mice with HF displayed obvious increases in intestinal permeability and plasma lipopolysaccharide (LPS) levels, which were accompanied by elevated expression of TLR4 in the brain and enhanced neuroinflammation. Treatment with the intestinal barrier protector IAP significantly attenuated neuroinflammation after HF while effectively increasing plasma LPS levels. TLR4-KO mice showed significant improvements in HF-induced neuroinflammation, which was not markedly affected by intestinal barrier inhibitors or protectors.

conclusionHF could induce intestinal barrier dysfunction and increase gut-to-blood translocation of LPS, which could further promote neuroinflammation through the TLR4 pathway.

Indexed as

heart failureintestinal barrierlipopolysaccharideneuroinflammationTLR4

Identifiers

PMID34421655
PMCPMC8378453
OpenAlexW3190709783

What OpenQuestion holds

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LicenceCC BY
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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.