Evidence map›Paper›PMID 35320391›Full record

ArticleHeart and vessels2022

Downregulation of lncRNA SNHG16 inhibits vascular smooth muscle cell proliferation and migration in cerebral atherosclerosis by targeting the miR-30c-5p/SDC2 axis.

Sheng-Nan Yang, Li-Ying Zhong, Ye-Hai Sun, Cong Wang, Wen-Juan Ru, Run-Zhi Liu, Wei Dai, Xiu-Mei Xie, Shun-Dong Li

Abstract read
PubMed Publisher
In one paragraph

Article in Heart and vessels, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 41% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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.

Sheng-Nan YangThe Departement of Geriatrics, The Third Hospital of Changsha, No. 176 West Labor Road, Changsha, 410000, Hunan Province, China.
Li-Ying ZhongThe Departement of Geriatrics, The Third Hospital of Changsha, No. 176 West Labor Road, Changsha, 410000, Hunan Province, China.
Ye-Hai SunThe Departement of Geriatrics, The Third Hospital of Changsha, No. 176 West Labor Road, Changsha, 410000, Hunan Province, China.
Cong WangThe Departement of Geriatrics, The Third Hospital of Changsha, No. 176 West Labor Road, Changsha, 410000, Hunan Province, China.
Wen-Juan RuThe Departement of Geriatrics, The Third Hospital of Changsha, No. 176 West Labor Road, Changsha, 410000, Hunan Province, China.
Run-Zhi LiuThe Departement of Geriatrics, The Third Hospital of Changsha, No. 176 West Labor Road, Changsha, 410000, Hunan Province, China.
Wei DaiThe Departement of Geriatrics, The Third Hospital of Changsha, No. 176 West Labor Road, Changsha, 410000, Hunan Province, China.
Xiu-Mei XieDivision of Cardiology, Xiangya Hospital, Central South University, Changsha, 410008, Hunan Province, China.
Shun-Dong LiThe Departement of Geriatrics, The Third Hospital of Changsha, No. 176 West Labor Road, Changsha, 410000, Hunan Province, China. lishundli85@163.com.ORCID http://orcid.org/0000-0002-0230-2219
Third Hospital of Changsha · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis (AS) is the basic lesion underlying the occurrence and development of cerebrovascular diseases. Abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a crucial role in AS. We aimed to explore the role of SNHG16 in AS and the molecular mechanism of VSMC involvement in the regulation of AS. The expression levels of SNHG16, miR-30c-5p and SDC2 were detected by qRT-PCR. CCK-8, wound healing and Transwell assays were used to assess ox-LDL-induced VSMC proliferation, migration, and invasion, respectively. Western blot analysis was used to detect SDC2 and MEK/ERK pathway-related protein levels. A dual-luciferase reporter assay confirmed the binding of SNHG16 with miR-30c-5p and miR-30c-5p with SDC2. SNHG16 and SDC2 expression was upregulated in patients with AS and ox-LDL-induced VSMCs, while miR-30c-5p was downregulated. Ox-LDL-induced VSMC proliferation and migration were increased, and the MEK/ERK signalling pathway was activated. MiR-30c-5p was targeted to SNHG16 and SDC2. Downregulating SNHG16 or upregulating miR-30c-5p inhibited ox-LDL-induced VSMC proliferation and migration and inhibited MEK/ERK signalling pathway activation. In contrast, downregulating miR-30c-5p or upregulating SDC2 reversed the effects of downregulating SNHG16 or upregulating miR-30c-5p. Furthermore, downregulating SDC2 inhibited ox-LDL-induced proliferation and migration of VSMCs and inhibited activation of the MEK/ERK signalling pathway, while upregulating lncRNA SNHG16 reversed the effects of downregulating SDC2. Downregulation of SNHG16 inhibited VSMC proliferation and migration in AS by targeting the miR-30c-5p/SDC2 axis. This study provides a possible therapeutic approach to AS.

Indexed as

AtherosclerosisIntracranial ArteriosclerosisMicroRNAsCell MovementCell ProliferationCells, CulturedDown-RegulationHumansLipoproteins, LDLMitogen-Activated Protein Kinase KinasesMuscle, Smooth, VascularMyocytes, Smooth MuscleRNA, Long NoncodingSyndecan-2Lipoproteins, LDLMicroRNAsMitogen-Activated Protein Kinase KinasesRNA, Long NoncodingSDC2 protein, humanSNHG16 lncRNA, humanSyndecan-2AtherosclerosisCell proliferationLncRNA SNHG16MigrationMiR-30c-5pSDC2

Identifiers

PMID35320391
OpenAlexW4220709725

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.