Evidence map›Paper›PMID 38705985›Full record

ArticleBMC cardiovascular disorders2024

miR-30a-5p attenuates hypoxia/reoxygenation-induced cardiomyocyte apoptosis by regulating PTEN protein expression and activating PI3K/Akt signaling pathway.

Guoxin Liang, Chang Guo, Hongyue Tang, Mingming Zhang

Abstract read
In one paragraph

Article in BMC cardiovascular disorders, 2024. 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
–field-weighted citation impact
1 · What the graph read from it

What it found

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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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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.

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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

4 authors.

Guoxin LiangDepartment of Laboratory Medicine, Nanjing BenQ Medical Center, The Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210000, China.
Chang GuoGraduate School, North China University of Science and Technology, Tangshan, Hebei, 063210, China.
Hongyue TangClinical Medicine Research Center, Hebei Key Laboratory of Metabolic Diseases, Hebei General Hospital, 348#, Hepingxi Road, PO Box: 050051, Shijiazhuang, 050051, China.
Mingming ZhangClinical Medicine Research Center, Hebei Key Laboratory of Metabolic Diseases, Hebei General Hospital, 348#, Hepingxi Road, PO Box: 050051, Shijiazhuang, 050051, China. zhangmm197612@hebmu.edu.cn.

Funding

Hebei Provincial Department of Science and Technology No. 20377776D
6 · The paper itself

Abstract

backgroundThis study was designed to investigate the mechanism by which miR-30a-5p mediates cardiomyocyte apoptosis after acute myocardial infarction (AMI) induced by hypoxia/reoxygenation (H/R).

methodsDifferentially expressed miRNAs were analyzed by RNA high-throughput sequencing in acute myocardial infarction (ST-elevation myocardial infarction) patients versus healthy individuals (controls). The H/R model was used to assess the regulatory mechanism of miRNAs in AMI. Lentivirus-associated vectors were used to overexpress or knock down miR-30a-5p in cellular models. The pathological mechanisms of miR-30a-5p regulating the development of acute myocardial infarction were serially explored by qPCR, bioinformatics, target gene prediction, dual luciferase, enzyme-linked immunosorbent assays (ELISAs) and Western blotting.

resultsThe results showed that the expression of miR-30a-5p was significantly increased in AMI patients and H9C2 cells. Hypoxia decreased cardiomyocyte survival over time, and reoxygenation further reduced cell survival. Bax and Phosphatase and tensin homolog (PTEN)were suppressed, while Bcl-2 was upregulated. Additionally, miR-30a-5p specifically targeted the PTEN gene. According to the GO and KEGG analyses, miR-30a-5p may participate in apoptosis by interacting with PTEN. The miR-30a-5p mimic decreased the expression of apoptosis-related proteins and the levels of the proinflammatory markers IL-1β, IL-6, and TNF-α by activating the PTEN/PI3K/Akt signaling pathway. Conversely, anti-miR-30a-5p treatment attenuated these effects. Additionally, silencing PTEN and anti-miR-30a-5p had opposite effects on H/R-induced cell apoptosis.

conclusionsmiR-30a-5p plays a crucial role in cardiomyocyte apoptosis after hypoxia-induced acute myocardial infarction. Our findings provide translational evidence that miR-30a-5p is a novel potential therapeutic target for AMI.

Indexed as

ApoptosisCell HypoxiaMicroRNAsMyocytes, CardiacPTEN PhosphohydrolaseSignal TransductionAnimalsCase-Control StudiesCell LineFemaleGene Expression RegulationHumansMaleMiddle AgedMyocardial InfarctionMyocardial Reperfusion InjuryMicroRNAsMIRN30a microRNA, humanMIRN30b microRNA, humanMIRN30 microRNA, ratPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanPten protein, ratApoptosisHypoxia/Reoxygenation (H/R)microRNA (miRNA)Phosphatase and Tensin Homolog (PTEN)Transcriptomics

Identifiers

PMID38705985
PMCPMC11070099

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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.