Evidence map›Paper›PMID 32695622›Full record

ArticleCardiovascular diagnosis and therapy2020

MicroRNA-363-3p serves as a diagnostic biomarker of acute myocardial infarction and regulates vascular endothelial injury by targeting KLF2.

Chao Gao, Hengbo Qian, Qibiao Shi, Hua Zhang

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Article in Cardiovascular diagnosis and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

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12citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Chao GaoDepartment of Emergency, Shanxian Central Hospital, Heze 274300, China.
Hengbo QianDepartment of Emergency, Shanxian Central Hospital, Heze 274300, China.
Qibiao ShiDepartment of Emergency, Shanxian Central Hospital, Heze 274300, China.
Hua ZhangDepartment of Emergency, Shanxian Central Hospital, Heze 274300, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myocardial infarction (AMI) is a serious cardiovascular disease. This study aimed to investigate the diagnostic value of microRNA-363-3p (miR-363-3p) in AMI patients and explore the effects of miR-363-3p on vascular endothelial injury in an AMI rat model.

methodsThe Expression of miR-363-3p was measured by quantitative real-time PCR. A receiver operating characteristic (ROC) curve was plotted to evaluate the diagnostic value of miR-363-3p in AMI patients. The biomarkers of endothelial injury were estimated using enzyme-linked immunosorbent assays, and the correlation of miR-363-3p with these markers was assessed. AMI rat model was constructed using coronary artery ligation, and the effects of miR-363-3p on endothelial injury and endothelial cell proliferation were analyzed.

resultsSerum expression of miR-363-3p was upregulated in the AMI patients compared with healthy controls. The increased serum miR-363-3p serves a candidate diagnostic biomarker of AMI. The correlation analysis indicated that serum miR-363-3p expression was positively correlated with the concentration of endothelial injury biomarkers in AMI patients. Furthermore, the increased endothelial injury biomarkers in AMI rats were all inhibited by the knockdown of miR-363-3p, and the cell proliferation of human umbilical vein endothelial cells was obviously enhanced by the reduction of miR-363-3p. The prediction results shown that Kruppel-like factor 2 (KLF2) is a target of miR-363-3p, and their interaction was proved using a luciferase reporter assay.

conclusionsCollectively, overexpression of miR-363-3p acts as a diagnostic biomarker for patients with AMI, and the downregulation of miR-363-3p improves AMI-associated endothelial injury by targeting KLF2, which indicated that miR-363-3p has a potential to develop the treatment of AMI.

Indexed as

acute myocardial infarction (AMI)Kruppel-like factor 2 (KLF2)MicroRNA-363-3p (miR-363-3p)proliferationvascular epithelia cells

Identifiers

PMID32695622
PMCPMC7369272

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