Evidence map›Paper›PMID 38376663›Full record

ArticleMolecular and cellular biochemistry2024

Circ_0004872 deficiency attenuates ox-LDL-induced vascular smooth muscle cell dysfunction by miR-424-5p-dependent regulation of FRS2.

Peng Qian, Xuanchao Cao, Qian Zhang, Meihua Gao, Xin Liu, Lijie Yan

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. LINC01088 Targets miR-195-5p to Promote Proliferation and Migration and Reduce Apoptosis in the Inhibition of Carotid Artery Stenosis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    Article
4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Peng Qian *Department of Geriatric Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, School of Clinical Medicine, Henan University, Zhengzhou, 450003, China.
Xuanchao Cao *Department of Geriatric Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, School of Clinical Medicine, Henan University, Zhengzhou, 450003, China.
Qian ZhangDepartment of Geriatric Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, School of Clinical Medicine, Henan University, Zhengzhou, 450003, China.
Meihua GaoDepartment of Geriatric Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, School of Clinical Medicine, Henan University, Zhengzhou, 450003, China.
Xin LiuDepartment of Geriatric Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, School of Clinical Medicine, Henan University, Zhengzhou, 450003, China.
Lijie YanHeart Center of Henan Provincial People's Hospital, Fuwai Central China Cardiovascular Hospital, Fuwai Central China Hospital of Zhengzhou University, No. 1 Fuwai Street, Zhengdong New District, Zhengzhou, 451464, China. yanlj003@zzu.edu.cn.

Funding

Henan Province High-Level Talent Internationalization Training Funding Project Yuke(2022)-3Henan Province Medical Science and Technology Joint Construction Project LHGJ20210110Henan Province Young and Middle-Aged Health Innovation Outstanding Young Talents Training Project YXKC2021051
6 · The paper itself

Abstract

Atherosclerosis (AS) is a pivotal pathological basis of cardiovascular and cerebrovascular diseases, and circular RNAs (circRNAs) has been disclosed to exert a vital part in the progression of AS. However, the functions of circ_0004872 in the progression of AS is indistinct. In this context, we aimed to elucidate the role of circ_0004872 and the potential mechanism in AS. The level of circ_0004872, miR-424-5p and fibroblast growth factor receptor substrate 2 (FRS2) was detected using quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was monitored by Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine (EDU) assays. The invasion and migration capabilities of VSMCs were tested by transwell assays and wound-healing assay, respectively. Western blot was adopted to check the protein levels of CyclinD1, Vimentin and FRS2. Dual-luciferase reporter and RNA immunoprecipitation assay were executed to manifest the interaction between miR-424-5p and circ_0004872 or FRS2. The level of circ_0004872 was increased in the serum samples of AS patients and ox-LDL-exposed VSMCs. Ox-LDL exposure triggered cell proliferation, invasion and migration ability of VSMCs. depletion of circ_0004872 partly weakened ox-LDL-mediated effects in VSMCs. Mechanistically, circ_0004872 functioned as a sponge of miR-424-5p, and miR-424-5p inhibition partly alleviated circ_0004872 deficiency-mediated influences in VSMCs. Additionally, miR-424-5p interacted with FRS2, and miR-424-5p constrained dysfunction in ox-LDL-stimulated VSMCs via reducing FRS2 level. Notably, circ_0004872 functioned as a sponge of miR-424-5p to elevate FRS2 expression. Circ_0004872 accelerated ox-LDL-induced damage via mediating miR-424-5p/FRS2 axis.

Indexed as

Adaptor Proteins, Signal TransducingLipoproteins, LDLMembrane ProteinsMicroRNAsMuscle, Smooth, VascularRNA, CircularAtherosclerosisCell MovementCell ProliferationHumansMaleMyocytes, Smooth MuscleAdaptor Proteins, Signal TransducingFRS2 protein, humanLipoproteins, LDLMembrane ProteinsMicroRNAsMIRN424 microrna, humanoxidized low density lipoproteinRNA, CircularASCirc_0004872FRS2miR-424-5pVSMCs

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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.