Evidence map›Paper›PMID 35794619›Full record

ArticleJournal of translational medicine2022

Extracellular vesicle miR-32 derived from macrophage promotes arterial calcification in mice with type 2 diabetes via inhibiting VSMC autophagy.

Jingsong Cao, Cong Chen, Qian Chen, Yan Gao, Zhibo Zhao, Qing Yuan, Anqi Li, Shiqi Yang, Yuqi He, Xuyu Zu and 1 more

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

Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.4field-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

25 citing papers in PubMed, 41 citations in OpenAlex.

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  13. MicroRNAs in diabetic macroangiopathy.Cardiovascular diabetology · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024
    Review
  20. 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

11 authors at 2 institutions in 1 country.

Jingsong Cao *The First Affiliated Hospital, Institute of Clinical Medicine, Department of Endocrinology and Metabolism, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China.ORCID 0000-0002-0133-282X
Cong Chen *The First Affiliated Hospital, Department of Laboratory Medicine, Hengyang Medical School, University of South China, Hengyang, 421000, China.
Qian Chen *The First Affiliated Hospital, Institute of Clinical Medicine, Department of Endocrinology and Metabolism, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China.
Yan GaoThe First Affiliated Hospital, Institute of Clinical Medicine, Department of Endocrinology and Metabolism, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China.
Zhibo ZhaoThe First Affiliated Hospital, Institute of Clinical Medicine, Department of Endocrinology and Metabolism, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China.
Qing YuanThe First Affiliated Hospital, Institute of Clinical Medicine, Department of Endocrinology and Metabolism, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China.
Anqi LiThe First Affiliated Hospital, Institute of Clinical Medicine, Department of Endocrinology and Metabolism, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China.
Shiqi YangThe First Affiliated Hospital, Institute of Clinical Medicine, Department of Endocrinology and Metabolism, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China.
Yuqi HeThe First Affiliated Hospital, Department of Laboratory Medicine, Hengyang Medical School, University of South China, Hengyang, 421000, China.
Xuyu ZuThe First Affiliated Hospital, Institute of Clinical Medicine, Department of Tumor Research, Hengyang Medical School, University of South China, Hengyang, 421000, China. zuxuyu0108@hotmail.com.
Jianghua LiuThe First Affiliated Hospital, Institute of Clinical Medicine, Department of Endocrinology and Metabolism, Hengyang Medical School, University of South China, Hengyang, 421000, Hunan, China. jianghua990@126.com.
University of South China · CNFirst Affiliated Hospital of University of South China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe development of diabetes vascular calcification (VC) is tightly associated with the inhibition of vascular smooth muscle cell (VSMC) autophagy. Previously, our team found that miR-32-5p (miR-32) promotes macrophage activation, and miR-32 is expressed at higher level in the plasma of patients with coronary calcification. However, whether miR-32 mediates the function of macrophages in type 2 diabetes (T2D) VC is still unclear.

methodsWild-type (WT) and miR-32

resultsWe found that high glucose conditions upregulate miR-32 expression in macrophages and their EVs. Importantly, macrophages and their EVs promote VSMC osteogenic differentiation and upregulate miR-32 expression in VSMCs. Moreover, miR-32 mimics transfection promoted osteogenic differentiation and inhibited autophagy in VSMCs. In vitro and in vivo experiments showed that Mef2d is the key target gene of miR-32 that inhibits VSMC autophagy. Furthermore, MS and transcriptome sequencing found that cGMP-PKG is an important signalling pathway by which Mef2d regulates VSMC autophagy. In addition, after T2D miR-32

conclusionsThese results reveal that EVs are the key pathway by which macrophages promote T2D VC, and that EVs miR-32 is a key cause of autophagy inhibition in VSMCs.

Indexed as

Diabetes Mellitus, Type 2Extracellular VesiclesMicroRNAsVascular CalcificationAnimalsAutophagyGlucoseMacrophagesMiceMuscle, Smooth, VascularOsteogenesisGlucoseMicroRNAsMIRN32 microRNA, mouseDiabetesEVsMacrophagemiR-32Vascular calcification

Identifiers

PMID35794619
PMCPMC9258116
OpenAlexW4283834402

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.