Evidence map›Paper›PMID 32106651›Full record

ArticleAnimal bioscience2021

Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens.

Yaling Zhu, Huirong Mao, Gang Peng, Qingjie Zeng, Qing Wei, Jiming Ruan, Jianzhen Huang

Open access · goldAbstract read
In one paragraph

Article in Animal bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Review
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  10. Protective Effects ofFrontiers in veterinary science · 2022
    Article
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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

7 authors at 2 institutions in 1 country.

Yaling ZhuCollege of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China.
Huirong MaoCollege of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China.
Gang PengCollege of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China.
Qingjie ZengCollege of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China.
Qing WeiCollege of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China.
Jiming RuanCollege of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China.
Jianzhen HuangCollege of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China.
Jiangxi Agricultural University · CNAnhui Medical University · CN

Funding

National Natural Science Foundation of China 31460648National Natural Science Foundation of China 31960690
6 · The paper itself

Abstract

objectiveTo explore the molecular mechanisms of fatty liver hemorrhagic syndrome (FLHS) in laying hens, an experiment was conducted to reveal the differences in histopathological observation and gene expression between FLHS group and normal group.

methodsWe compared the histopathological difference using hematoxylin and eosin staining and proceeded with RNA sequencing of adipose tissue to search differentially expressed genes and enriched biological processes and pathways. Then we validated the mRNA expression levels by real-time polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay.

resultsWe identified 100 differentially expressed transcripts corresponding to 66 genes (DEGs) were identified between FLHS-affected group and normal group. Seven DEGs were significantly enriched in the immune response process and lipid metabolic process, including phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (IL-6), ciliary neurotrophic factor (CNTF), and suppressor of cytokine signaling 3 (SOCS3). And these genes could be the targets of immune response and be involved in metabolic homeostasis during the process of FLHS in laying hens. Based on functional categories of the DEGs, we further proposed a model to explain the etiology and pathogenesis of FLHS. IL-6 and SOCS3 mediate inflammatory responses and the satiety hormone of leptin, induce dysfunction of Jak-STAT signaling pathway, leading to insulin resistance and lipid metabolic disorders. Conversely, CNTF may reduce tissue destruction during inflammatory attacks and confer protection from inflammation-induced insulin resistance in FLHS chickens.

conclusionThese findings highlight the therapeutic implications of targeting the JAK-STAT pathway. Inhibition of IL6 and SOCS3 and facilitation of CNTF could serve as a favorable strategy to enhance insulin action and improve glucose homoeostasis, which are of importance for treating obesity-related disorders for chickens.

Indexed as

ChickenDifferentially Expressed GenesFatty Liver Hemorrhagic SyndromeJAK-STAT PathwayRNA-Seq

Identifiers

PMID32106651
PMCPMC7888496
OpenAlexW3008239900

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.