Evidence map›Paper›PMID 31237148›Full record

ArticleDrug delivery2019

Up-regulation of MIAT aggravates the atherosclerotic damage in atherosclerosis mice through the activation of PI3K/Akt signaling pathway.

Guoqiang Sun, Yubo Li, Zhiyong Ji

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Drug delivery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Role of LncRNA MIAT in Diabetic Complications.Current medicinal chemistry · 2024
    Review
  7. Article
  8. Article
  9. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. TCM Regulates PI3K/Akt Signal Pathway to Intervene Atherosclerotic Cardiovascular Disease.Evidence-based complementary and alternative medicine : eCAM · 2021
    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

3 authors at 1 institution in 1 country.

Guoqiang Suna Department of Cardiology , The First Hospital of Jilin University , Changchun , PR China.
Yubo Lib Department of Pediatrics , Medical College , Changchun , PR China.
Zhiyong Jic Department of Critical Care Medicine , The First Hospital of Jilin University , Changchun , PR China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study is performed to elucidate the role of long non-coding RNA myocardial infarction associated transcript (lncRNA MIAT) in vulnerable plaque formation in rats with atherosclerosis (AS) through the regulation of the PI3K/Akt signaling pathway. The mice model of AS was established, and the successful modeled AS mice were treated with overexpressed MIAT and silenced MIAT. The levels of blood lipids, atherosclerotic plaques (AP) formation, the lipid content, collagen content, apoptosis of aortic cells, angiogenesis as well as the expression of inflammatory factors, such as tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were determined through a series of experiments. MIAT was found to be upregulated in AS. Additionally, MIAT up-regulated the levels of blood lipids, promoted AP formation, increased the lipid content and decreased the collagen content of AP, promoted the apoptosis of aortic cells in AS mice by activating the PI3K/Akt signaling pathway. Meanwhile, MIAT was determined to promote angiogenesis as well as the expression of inflammatory factors (IL-1β, IL-6, and TNF-α) in AS mice through the activation of the PI3K/Akt signaling pathway. Furthermore, MIAT activated the PI3K/Akt signaling pathway to participate in AS progression. Our study suggests that upregulation of MIAT can aggravate AS injury in AS mice via the activation of the PI3K/Akt signaling pathway, which could provide a novel target for the treatment of AS.

Indexed as

AnimalsApoptosisAtherosclerosisDisease Models, AnimalInterleukin-1betaInterleukin-6MaleMiceMyocardial InfarctionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRNA, Long NoncodingSignal TransductionTumor Necrosis Factor-alphaUp-RegulationInterleukin-1betaInterleukin-6Miat long non-coding RNAPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingTumor Necrosis Factor-alphaatherosclerosisatherosclerotic damageLncRNA MIATPI3K/Akt signaling pathway

Identifiers

PMID31237148
PMCPMC6598488
OpenAlexW2956133393

What OpenQuestion holds

Textmetadata
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.