Evidence map›Paper›PMID 38953358›Full record

ArticlemBio2024

Butyrate promotes visceral hypersensitivity in IBS model via mast cell-derived DRG neuron lincRNA-01028-PKC-TRPV1 pathway.

Ying-Jie Li, Jing Li, Cong Dai

Abstract read
In one paragraph

Article in mBio, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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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

3 authors.

Ying-Jie LiDepartment of Gastroenterology, First Affiliated Hospital, Jinzhou Medical University, Jinzhou City, Liaoning Province, China.
Jing LiDepartment of Gastroenterology, First Affiliated Hospital, Jinzhou Medical University, Jinzhou City, Liaoning Province, China.ORCID 0000-0001-8283-5789
Cong DaiDepartment of Gastroenterology, First Hospital of China Medical University, Shenyang City, Liaoning Province, China.ORCID 0000-0003-1317-183X

Funding

Department of Science and Technology of Liaoning Province () No 2020-BS-251MOST | National Natural Science Foundation of China (NSFC) No 82270571
6 · The paper itself

Abstract

Emerging evidence indicates that gut dysbiosis is involved in the pathogenesis of visceral hypersensitivity (VH). However, how gut microbiota contributes to the development of VH is unknown. Here, we sought to examine the signal transduction pathways from gut to dorsal root ganglion (DRG) responsible for this. Therefore, abdominal withdrawal reflex (AWR) scores, fecal output, fecal water content, and total gastrointestinal transit time (TGITT) were assessed in Con rats, VH rats, rats treated with NaB, and VH rats treated with VSL#3. Fecal microbiota and its metabolite (short-chain fatty acids, SCFAs), mast cell degranulation in colon, lincRNA-01028, miR-143, and protease kinase C (PKC) and TRPV1 expression in DRGs were further detected. VH rats showed an increased fecal water content, a shortened TGITT, an increased abundance of Clostridium

Indexed as

ButyratesDisease Models, AnimalGanglia, SpinalIrritable Bowel SyndromeMast CellsProtein Kinase CRats, Sprague-DawleyTRPV Cation ChannelsAnimalsGastrointestinal MicrobiomeMaleNeuronsRatsSignal TransductionButyratesProtein Kinase CTrpv1 protein, ratTRPV Cation Channelsbutyratedorsal root ganglionmast cellshort-chain fatty acidsvisceral hypersensitivity

Identifiers

PMID38953358
PMCPMC11323730

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.