Evidence map›Paper›PMID 38553251›Full record

ArticleAlcohol, clinical & experimental research2024

Network meta-analysis of the molecular mechanisms and signaling pathways underlying alcohol-induced thymic atrophy.

Tatiana Rengifo, Muhammed Bishir, Wenfei Huang, Marylynn Snyder, Sulie L Chang

Open access · goldAbstract read
In one paragraph

Article in Alcohol, clinical & experimental research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.5field-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

3 citing papers in PubMed, 6 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

5 authors at 1 institution in 1 country.

Tatiana RengifoInstitute of NeuroImmune Pharmacology, Seton Hall University, South Orange, New Jersey, USA.ORCID https://orcid.org/0000-0001-9223-9948
Muhammed BishirInstitute of NeuroImmune Pharmacology, Seton Hall University, South Orange, New Jersey, USA.
Wenfei HuangInstitute of NeuroImmune Pharmacology, Seton Hall University, South Orange, New Jersey, USA.
Marylynn SnyderDepartment of Biological Sciences, Seton Hall University, South Orange, New Jersey, USA.
Sulie L ChangInstitute of NeuroImmune Pharmacology, Seton Hall University, South Orange, New Jersey, USA.ORCID https://orcid.org/0000-0003-3865-4280
Seton Hall University · US

Funding

Methylation in binge ethanol-induced spleen atrophy in adolescent ratsU01AA025964 · NIAAA · SETON HALL UNIVERSITY · PI CHANG, SULIE L. · 2018 to 2022
$1.6M
Involvement of microglial α7AChR in binge alcohol modulation of gut dysbiosisR21AA029925 · NIAAA · SETON HALL UNIVERSITY · PI CHANG, SULIE L., KHAN, MOHAMMED A. S. · 2022 to 2023
$402k
Effects of binge ethanol on neuroinflammation and neurodegeneration with high fat dietsR21AA030221 · NIAAA · SETON HALL UNIVERSITY · PI CHANG, SULIE L., ZHOU, HEPING · 2023 to 2023
$392k
NIAAA NIH HHS R21 AA029925NIAAA NIH HHS R21 AA030221NIAAA NIH HHS U01 AA025964NIH HHS AA025964NIH HHS AA029925NIH HHS AA030221
6 · The paper itself

Abstract

backgroundThymic atrophy is characterized by loss of thymocytes, destruction of thymic architecture, and a subsequent decrease in naïve T cells with compromised immunity. Thymic atrophy occurs during aging. Environmental factors including alcohol misuse also induce thymic atrophy. Despite the link between alcohol misuse and thymic atrophy, the underlying mechanism is understudied. We aimed to identify molecules and signaling pathways that underly alcohol-induced thymic atrophy during aging.

methodsF344 rats were given 3-day binge-ethanol (4.8 g/kg/day; 52% w/v; i.g.) and the thymus was collected and weighed. Molecular mechanisms underlying ethanol-induced thymic atrophy were investigated by network meta-analysis using the QIAGEN Ingenuity Pathway Analysis (IPA). The molecules associated with ethanol were identified from the QIAGEN Knowledge Base (QKB) and those associated with thymic atrophy were identified from QKB and Mouse Genome Informatics (MGI). Aging-mediated Differential Expression Genes (DEGs) from mouse thymocytes were obtained from the Gene Expression Omnibus (GEO) database (GSE132136). The relationship between the molecules and associated signaling pathways were studied using IPA.

resultsBinge-ethanol decreased thymic weight in F344 rats. Our meta-analysis using IPA identified molecules commonly shared by ethanol and thymic atrophy through which simulation with ethanol increased thymic atrophy. We then obtained aging-mediated DEGs from the atrophied thymocytes. We found that ethanol contributed to thymic atrophy through modulation of the aging-mediated DEGs. Our network meta-analysis suggests that ethanol may augment thymic atrophy through increased expression of cytokines (e.g., IL-6, IL-17A and IL-33) along with their regulators (e.g., STAT1 and STAT3).

conclusionsExposure to alcohol may augment thymic atrophy by altering the activity of key inflammatory mediators, such as STAT family members and inflammatory cytokines. These findings provide insights into the signaling pathways and upstream regulators that underly alcohol-induced thymic atrophy during aging, suggesting that alcohol consumption could prepone thymic atrophy.

Indexed as

aging‐mediated thymus atrophyinflammatory cytokinesingenuity pathway analysisQIAGEN Knowledge BaseSTAT

Identifiers

PMID38553251
PMCPMC11161038
OpenAlexW4393344385

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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.