Evidence map›Paper›PMID 26974319›Full record

ArticlePloS one2016

Folic Acid Represses Hypoxia-Induced Inflammation in THP-1 Cells through Inhibition of the PI3K/Akt/HIF-1α Pathway.

Xiaoyan Huang, Zhiying He, Xinwei Jiang, Mengjun Hou, Zhihong Tang, Xiaozhou Zhen, Yuming Liang, Jing Ma

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
2.1field-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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 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

8 authors at 1 institution in 1 country.

Xiaoyan HuangDepartment of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, P. R. China.
Zhiying HeDepartment of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, P. R. China.
Xinwei JiangDepartment of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, P. R. China.
Mengjun HouExperimental and Teaching Center for public health, School of Public Health, Sun Yat-Sen University, Guangzhou, P. R. China.
Zhihong TangExperimental and Teaching Center for public health, School of Public Health, Sun Yat-Sen University, Guangzhou, P. R. China.
Xiaozhou ZhenDepartment of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, P. R. China.
Yuming LiangDepartment of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, P. R. China.
Jing MaDepartment of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, P. R. China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Though hypoxia has been implicated as a cause of inflammation, the underlying mechanism is not well understood. Folic acid has been shown to provide protection against oxidative stress and inflammation in patients with cardiovascular disease and various models approximating insult to tissue via inflammation. It has been reported that hypoxia-induced inflammation is associated with oxidative stress, upregulation of hypoxia-inducible factor 1-alpha (HIF-1α), and production of pro-inflammatory molecules. Whether folic acid protects human monocytic cells (THP-1 cells) against hypoxia-induced damage, however, remains unknown. We used THP-1 cells to establish a hypoxia-induced cellular injury model. Pretreating THP-1 cells with folic acid attenuated hypoxia-induced inflammatory responses, including a decrease in protein and mRNA levels of interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α), coupled with increased levels of IL-10. Folic acid also reduced hypoxia-induced Akt phosphorylation and decreased nuclear accumulation of HIF-1α protein. Both LY294002 (a selective inhibitor of phosphatidyl inositol-3 kinase, PI3K) and KC7F2 (a HIF-1α inhibitor) reduced levels of hypoxia-induced inflammatory cytokines. We also found that insulin (an Akt activator) and dimethyloxallyl glycine (DMOG, a HIF-1α activator) induced over-expression of inflammatory cytokines, which could be blocked by folic acid. Taken together, these findings demonstrate how folic acid attenuates the hypoxia-induced inflammatory responses of THP-1 cells through inhibition of the PI3K/Akt/HIF-1α pathway.

Indexed as

Cell HypoxiaCell LineCytokinesCytoprotectionFolic AcidGene Expression RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitInflammationInflammation MediatorsModels, BiologicalPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktReal-Time Polymerase Chain ReactionRNA, MessengerCytokinesFolic AcidHypoxia-Inducible Factor 1, alpha SubunitInflammation MediatorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, MessengerVascular Endothelial Growth Factor A

Identifiers

PMID26974319
PMCPMC4790958
OpenAlexW2300936249

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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.