Evidence map›Paper›PMID 32367412›Full record

ArticleInflammation2020

SMILR Aggravates the Progression of Atherosclerosis by Sponging miR-10b-3p to Regulate KLF5 Expression.

Huaqing Li, Zhiyu Pan, Qian Chen, Zhen Yang, Dongbing Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Establishment of a lncRNA-miRNA-mRNA network in a rat model of atrial fibrosis by whole transcriptome sequencing.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2022
    Article
  8. Article
  9. Article
  10. Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022
    Review
  11. Article
  12. Roles of Krüppel-like factor 5 in kidney disease.Journal of cellular and molecular medicine · 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

5 authors at 2 institutions in 1 country.

Huaqing LiDepartment of Vascular Surgery, Minhang Hospital, Fudan University, No. 39 Xinling Road, Minhang District, 201199, Shanghai, China.
Zhiyu PanDepartment of Vascular Surgery, Minhang Hospital, Fudan University, No. 39 Xinling Road, Minhang District, 201199, Shanghai, China. panzyvs@hotmail.com.
Qian ChenDepartment of Vascular Surgery, Minhang Hospital, Fudan University, No. 39 Xinling Road, Minhang District, 201199, Shanghai, China.
Zhen YangDepartment of Vascular Surgery, Minhang Hospital, Fudan University, No. 39 Xinling Road, Minhang District, 201199, Shanghai, China.
Dongbing ZhangDepartment of Vascular Surgery, Minhang Hospital, Fudan University, No. 39 Xinling Road, Minhang District, 201199, Shanghai, China.
Minhang District Central Hospital · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the past few decades, long noncoding RNAs (lncRNAs) have been widely accepted to be involved in various diseases, and smooth muscle enriched long noncoding RNA (SMILR) was reported to participate in the proliferation of vascular smooth muscle cells (VSMCs). Nevertheless, the molecular mechanisms of SMILR in atherosclerosis (AS) have not been fully explored. In this study, VSMCs and human mononuclear cells (U937) treated with oxidized low-density lipoprotein (ox-LDL) were used as cell models of AS. We found that the expression of SMILR was upregulated in the serum of AS patients and ox-LDL-induced AS cell models. SMILR knockdown inhibited cell proliferation while increasing cell apoptosis in the AS cell models. In addition, SMILR acted as a sponge for miR-10b-3p, and miR-10b-3p counteracted SMILR-mediated regulation of AS. Moreover, we confirmed that miR-10b-3p could bind with KLF5, and SMILR regulated KLF5 expression by competitively binding miR-10b-3p. Furthermore, miR-10b-3p modulated cell proliferation and apoptosis in AS by targeting KLF5. Finally, miR-10b-3p regulated AS progression in vivo by targeting KLF5. Overall, our study demonstrated that SMILR participated in the progression of AS by targeting the miR-10b-3p/KLF5 axis, which may provide some clues for future studies of AS.

Indexed as

Disease ProgressionAnimalsAtherosclerosisCell ProliferationGene ExpressionHumansKruppel-Like Transcription FactorsMiceMicroRNAsMuscle, Smooth, VascularMyocytes, Smooth MuscleRNA, Long NoncodingU937 CellsKLF5 protein, humanKruppel-Like Transcription FactorsMicroRNAsMIRN10 microRNA, humanRNA, Long NoncodingASKLF5miR-10b-3pSMILR

Identifiers

PMID32367412
OpenAlexW3022202700

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.