Evidence map›Paper›PMID 34498594›Full record

ArticleAnatolian journal of cardiology2021

MiRNA-130a promotes inflammation to accelerate atherosclerosis via the regulation of proliferator-activated receptor γ (PPARγ) expression.

Fengtong Liu, Yali Liu, Yuqing Du, Youshan Li

Open access · diamondAbstract read
In one paragraph

Article in Anatolian journal of cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Therapeutic effects of combining curcumin and swimming in osteoarthritis using a rat model.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
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 2 institutions in 1 country.

Fengtong LiuDepartment of Peripheral Vascular, Dongzhimen Hospital, Beijing University of Chinese Medicine; Beijing-China.
Yali LiuDepartment of Peripheral Vascular, Dongzhimen Hospital, Beijing University of Chinese Medicine; Beijing-China.
Yuqing DuDepartment of Peripheral Vascular, Dongzhimen Hospital, Beijing University of Chinese Medicine; Beijing-China.
Youshan LiDepartment of Peripheral Vascular, Dongzhimen Hospital, Beijing University of Chinese Medicine; Beijing-China.
Beijing University of Chinese Medicine · CNDongzhimen Hospital Affiliated to Beijing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIn this study, we aimed to evaluate the possible function of miR-130a in atherosclerosis (AS), protection against AS, and its molecular biological mechanism.

methodsApoe-/- mice were fed a high-fat diet as the AS mice model. Human umbilical vein endothelial cells (HUVECs) were used as in vitro model. Serum samples or cells were used to measure the expression of inflammation. Serum samples or cells were used to determine MiRNA expression profiles using the edgeR tool from Bioconductor. Western Blot analysis was used to assess protein expressions of proliferator-activated receptor γ (PPARγ) and nuclear factor (NF)-κB.

resultsMiRNA-130a expression was up-regulated in atherosclerotic mice. In addition, over-expression of miRNA-130a promoted inflammation factors [tumor necrosis factor (TNF)-α and interleukin (IL)-1β, IL-6, and IL-8] in the in vitro model of AS. However, down-regulation of miRNA-130a reduced inflammation (suppressed TNF-α, IL-1β, IL-6 and IL-8) in the in vitro model. Furthermore, over-expression of miRNA-130a could also suppress the protein expression of PPARγ and induce NF-κB protein expression in the in vitro model. However, suppression of miRNA-130a induced the protein expression of PPARγ and suppressed NF-κB protein expression in the in vitro model of AS. Activation of PPARγ reduced the pro-inflammatory effects of miRNA-130a on the AS-induced in vitro model.

conclusionThese results strongly support that miRNA-130a suppression can protect against atherosclerosis through inhibiting inflammation by regulating the PPARγ/ NF-κB expression.

Indexed as

AtherosclerosisMicroRNAsAnimalsHumansHuman Umbilical Vein Endothelial CellsInflammationMicePeroxisome Proliferator-Activated ReceptorsPPAR gammaMicroRNAsPeroxisome Proliferator-Activated ReceptorsPPAR gammaPparg protein, mouse

Identifiers

PMID34498594
PMCPMC8443196
OpenAlexW3198560691

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.