Evidence map›Paper›PMID 35288486›Full record

ArticleAging2022

miRNA-29a inhibits atherosclerotic plaque formation by mediating macrophage autophagy via PI3K/AKT/mTOR pathway.

Weihua Shao, Suxing Wang, Xiaoxi Wang, Lixia Yao, Xiaoye Yuan, Dai Huang, Bonan Lv, Yuquan Ye, Hongyuan Xue

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. miR-29a-3p/Renal failure · 2025
    Article
  4. mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025
    Review
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  6. Review
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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

9 authors at 2 institutions in 1 country.

Weihua ShaoSecond Department of Geriatrics, Hebei Medical University and Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Suxing WangSecond Department of Geriatrics, Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Xiaoxi WangMedical Examination Center, Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Lixia YaoSecond Department of Geriatrics, Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Xiaoye YuanSecond Department of Geriatrics, Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Dai HuangUltrasound Department, Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Bonan LvVascular Surgery, Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Yuquan YeUltrasound Department, Hebei Medical University and Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Hongyuan XueUltrasound Department, Hebei General Hospital, Shijiazhuang 050051, Hebei, China.
Hebei General Hospital · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundmiR-29a plays a vital role in AS, but the relationship between the miR-29a-targeted PI3K signaling pathway and AS remains unclear. Therefore, this study was carried out.

methodsGene expression profiles from the GEO database containing AS samples were analyzed. ApoE

resultsDEGs were identified from GSE137578, GSE132651, GSE113969, GSE43292, and GSE97210 datasets. It was found that there were targeted binding sites between miR-29a and PIK3CA. Besides, GO and KEGG analysis demonstrated that autophagy was an enriched pathway in AS. Later, PPI network was depicted, and hub genes were then determined. The results revealed that miR-29a suppressed the areas of plaques and lesional macrophages, but had no impact on VSMCs. TEM results showed the organelles pyknosis of lesional macrophages damaged morphological changes. Furthermore, miR-29a amplified the M2-like macrophages but suppressed the polarization of M1-like macrophages in atherosclerotic plaques. According to mouse and RAW 264.7 cell experiments, miR-29a significantly inhibited the protein expressions of PI3K, p-PI3K, p-AKT, and p-mTOR, which were consistent with the increased expressions of autophagy-related proteins, Beclin 1 and LC3II. However, the miR-29a suppression exhibited the contrary results.

conclusionMiR-29a elevation induces the increase of autophagy by down-regulating the PI3K/AKT/mTOR pathway in the progression of AS, indicating that miR-29a is a novel therapeutic strategy for AS.

Indexed as

AtherosclerosisMicroRNAsPlaque, AtheroscleroticAnimalsAutophagyMacrophagesMicePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesatherosclerosisatheroscleroticmacrophagemiR-29aPI3K/AKT/mTORplaque

Identifiers

PMID35288486
PMCPMC8954956
OpenAlexW4220976008

What OpenQuestion holds

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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.