Evidence map›Paper›PMID 31938226›Full record

ArticleInternational journal of clinical and experimental pathology2018

Fibroblast growth factor 21 attenuates inflammation and oxidative stress in atherosclerotic rat via enhancing the Nrf1-ARE signaling pathway.

Haizhen Jia, Jing Cheng, Qi Zhou, Jun Peng, Yunhong Pan, Hongyan Han

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

22 citing papers in PubMed, 22 citations in OpenAlex.

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  13. Adipokines, adiposity, and atherosclerosis.Cellular and molecular life sciences : CMLS · 2022
    Review
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  15. Article
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  17. Article
  18. Article
  19. Review
  20. Adipokines and Inflammation: Focus on Cardiovascular Diseases.International journal of molecular sciences · 2020
    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

6 authors at 1 institution in 1 country.

Haizhen JiaDepartment of Cardiology, Tianyou Hospital Affiliated to Wuhan University of Science and Technology Wuhan, Hubei, China.
Jing ChengDepartment of Cardiology, Tianyou Hospital Affiliated to Wuhan University of Science and Technology Wuhan, Hubei, China.
Qi ZhouDepartment of Cardiology, Tianyou Hospital Affiliated to Wuhan University of Science and Technology Wuhan, Hubei, China.
Jun PengDepartment of Cardiology, Tianyou Hospital Affiliated to Wuhan University of Science and Technology Wuhan, Hubei, China.
Yunhong PanDepartment of Cardiology, Tianyou Hospital Affiliated to Wuhan University of Science and Technology Wuhan, Hubei, China.
Hongyan HanDepartment of Cardiology, Tianyou Hospital Affiliated to Wuhan University of Science and Technology Wuhan, Hubei, China.
Wuhan University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation and oxidative stress are associated with atherosclerotic progression. Fibroblast growth factor 21 (FGF21), a regulator of energy metabolism, has been reported to suppress the pathogenesis of atherosclerosis. However, the mechanism of anti-atherosclerotic effects of FGF21 remains unclear and needs to be further investigated. Transcription factor NF-E2-related 2 (Nrf2), a sensitive regulator of oxidative stress, is also associated with atherosclerotic progression. In this study, we investigated whether up-regulation of FGF21 affected inflammation and oxidative stress in atherosclerotic rats and whether the Nrf2-signaling pathway was involved in FGF21-mediated effects. Pathological changes were detected in arterial tissues of rats, and the expression of inflammatory and oxidative stress indicators, vascular endothelial markers, and Nrf2-signaling related protein were measured in the serum or/and arterial tissues of rats. As a result, expression of FGF21 and Nrf2-ARE signaling related proteins were markedly suppressed in arterial tissues of model rats. Thickness of endarteria and infiltrating cells obviously increased in atherosclerotic rats, whereas the increase of FGF21 expression could decrease thickness of endarteria. Moreover, the levels of ET-1, MDA, MCP-1, ICAM-1 and VCAM-1 were significantly higher in model rats than that in normal rats, whereas the levels of NO, GSH and T-AOC were significantly lower. Compared with model rats, up-regulation of FGF21 could increase the expression of Nrf2-ARE signaling related proteins and the level of anti-oxidative indicators, decrease the levels of endothelial dysfunction, and reduce inflammatory indicators. Down-regulation of FGF21 could reverse these actions. Therefore FGF21 reduces inflammation and oxidative stress in atherosclerotic rats via Nrf2-ARE signaling pathway.

Indexed as

atherosclerosisFGF21inflammationNrf2oxidative stress

Identifiers

PMID31938226
PMCPMC6958096
OpenAlexW3026141250

What OpenQuestion holds

Textmetadata
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.