Evidence map›Paper›PMID 32218693›Full record

ArticleInternational journal of medical sciences2020

ACSL1 affects Triglyceride Levels through the PPARγ Pathway.

Tingting Li, Xiangdong Li, Heyu Meng, Lili Chen, Fanbo Meng

Open access · goldAbstract read
In one paragraph

Article in International journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

55 citing papers in PubMed, 75 citations in OpenAlex.

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  15. Frontiers in nutrition · 2025
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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 2 institutions in 1 country.

Tingting LiDepartment of Cardiology China-Japan Union Hospital of Jilin University, Changchun, China 130033.
Xiangdong LiDepartment of Cardiology China-Japan Union Hospital of Jilin University, Changchun, China 130033.
Heyu MengDepartment of Cardiology China-Japan Union Hospital of Jilin University, Changchun, China 130033.
Lili ChenDepartment of Cardiology China-Japan Union Hospital of Jilin University, Changchun, China 130033.
Fanbo MengDepartment of Cardiology China-Japan Union Hospital of Jilin University, Changchun, China 130033.
Jilin University · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In clinical cohort studies, high expression of long-chain acyl-coenzyme A synthetases 1 (ACSL1 gene) in peripheral white blood cells of patients with acute myocardial infarction (AMI) has been utilized as molecular markers of myocardial infarction diagnosis. The plasma triglyceride level of AMI patients is significantly higher than that of healthy individuals. We hypothesized that the high expression of ACSL1 increases the level of triglyceride, which is one of the pathogenesis of AMI promoted by ACSL1. In this report, cell culture based methods were adopted to test the hypothesis and further investigate the effect and mechanism of ACSL1 on lipid metabolism. In this study, liver cells of healthy individuals were cultured, the overexpression and the knockdown vectors of ACSL1 were constructed and transfected into liver cells. The transfection was verified at the mRNA and protein level. Intracellular triglyceride content was quantitatively analyzed using ELISA. Changes of genes related to lipid metabolism were subsequently measured through PCR array. Overexpression of ACSL1 led to higher gene expression and protein levels compared to control and the triglyceride content was significantly increased in overexpressing cells. The expression level of fatty acid oxidation pathway PPARγ was significantly down-regulated compared with the control group, as were genes associated with fatty acid synthesis pathways: SREBP1, ACC, FAS, and SCD1. ACSL1 knockdown decreased the content of triglyceride whereas PPARγ was up-regulated and SREBP1, ACC, FAS, and SCD1 were down-regulated compared with the control group. In summary, high expression of ACSL1 reduced fatty acid β-oxidation through the PPARγ pathway, thereby increasing triglyceride levels.

Indexed as

Acetyl-CoA CarboxylaseBiomarkersCoenzyme A LigasesGene Expression RegulationGenetic VectorsHumansLipid MetabolismLiverMyocardial InfarctionPPAR gammaPrimary Cell CultureStearoyl-CoA DesaturaseSterol Regulatory Element Binding Protein 1TransfectionTriglyceridesACACA protein, humanAcetyl-CoA CarboxylaseACSL1 protein, humanBiomarkersCoenzyme A LigasesPPAR gammaPPARG protein, humanSCD1 protein, humanSREBF1 protein, humanStearoyl-CoA DesaturaseSterol Regulatory Element Binding Protein 1TriglyceridesACSL1Lipid MetabolismMyocardium InfarctionPPARrTriglyceride

Identifiers

PMID32218693
PMCPMC7085263
OpenAlexW3012719501

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.