Evidence map›Paper›PMID 33960626›Full record

ArticleJournal of cellular and molecular medicine2021

Fructose-1,6-bisphosphatase aggravates oxidative stress-induced apoptosis in asthma by suppressing the Nrf2 pathway.

Jiapeng Hu, Jia Wang, Chunlu Li, Yunxiao Shang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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  18. Ferroptosis triggers airway inflammation in asthma.Therapeutic advances in respiratory disease
    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

4 authors at 1 institution in 1 country.

Jiapeng HuDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.
Jia WangDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.
Chunlu LiDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.
Yunxiao ShangDepartment of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.ORCID 0000-0003-4110-1177
China Medical University · CN

Funding

The 345 Talent Project of Shengjing Hospital of China Medical University, Shenyang, China M0421
6 · The paper itself

Abstract

Asthma is a chronic airway disease that causes excessive inflammation, oxidative stress, mucus production and bronchial epithelial cell apoptosis. Fructose-1,6-bisphosphatase (Fbp1) is one of the rate-limiting enzymes in gluconeogenesis and plays a critical role in several cancers. However, its role in inflammatory diseases, such as asthma, is unclear. Here, we examined the expression, function and mechanism of action of Fbp1 in asthma. Gene Expression Omnibus (GEO) data sets revealed that Fbp1 was overexpressed in a murine model of asthma and in interleukin (IL)-4- or IL-13-stimulated bronchial epithelial cells. We confirmed the findings in an animal model as well as Beas-2B and 16HBE cells. In vitro investigations revealed that silencing of Fbp1 reduced apoptosis and the proportion of cells in the G2/M phase, whereas overexpression led to increases. Fbp1 knock-down inhibited oxidative stress by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, whereas Fbp1 overexpression aggravated oxidative stress by suppressingthe Nrf2 pathway. Moreover, the Nrf2 pathway inhibitor ML385 reversed the changes caused by Fbp1 inhibition in Beas-2B and 16HBE cells. Collectively, our data indicate that Fbp1 aggravates oxidative stress-induced apoptosis by suppressing Nrf2 signalling, substantiating its potential as a novel therapeutic target in asthma.

Indexed as

Gene Expression RegulationOxidative StressAnimalsAsthmaFemaleFructose-BisphosphataseMiceMice, Inbred BALB CNF-E2-Related Factor 2OvalbuminFructose-BisphosphataseNfe2l2 protein, mouseNF-E2-Related Factor 2OvalbuminapoptosisasthmaFbp1oxidative stress

Identifiers

PMID33960626
PMCPMC8178285
OpenAlexW3157545398

What OpenQuestion holds

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LicenceCC BY
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.