MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1

Myocardial infarction (MI) is a leading cause of mortality. To better understand its molecular and cellular mechanisms, we used bioinformatic tools and molecular experiments to explore the pathogenesis and prognostic markers. Differential gene expression analysis was conducted using GSE60993 and GSE...

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Autores principales: Lin, Hao, Chu, Jiapeng, Yuan, Deqiang, Wang, Kangwei, Chen, Fei, Liu, Xuebo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Research
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10512505/
https://www.ncbi.nlm.nih.gov/pubmed/37730550
http://dx.doi.org/10.1186/s12872-023-03481-8
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author Lin, Hao
Chu, Jiapeng
Yuan, Deqiang
Wang, Kangwei
Chen, Fei
Liu, Xuebo
author_facet Lin, Hao
Chu, Jiapeng
Yuan, Deqiang
Wang, Kangwei
Chen, Fei
Liu, Xuebo
author_sort Lin, Hao
collection PubMed
description Myocardial infarction (MI) is a leading cause of mortality. To better understand its molecular and cellular mechanisms, we used bioinformatic tools and molecular experiments to explore the pathogenesis and prognostic markers. Differential gene expression analysis was conducted using GSE60993 and GSE66360 datasets. Hub genes were identified through pathway enrichment analysis and PPI network construction, and four hub genes (AQP9, MMP9, FPR1, and TREM1) were evaluated for their predictive performance using AUC and qRT-PCR. miR-206 was identified as a potential regulator of TREM1. Finally, miR-206 was found to induce EC senescence and ER stress through upregulating mitochondrial ROS levels via TREM1. These findings may contribute to understanding the pathogenesis of MI and identifying potential prognostic markers. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12872-023-03481-8.
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spelling pubmed-105125052023-09-22 MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1 Lin, Hao Chu, Jiapeng Yuan, Deqiang Wang, Kangwei Chen, Fei Liu, Xuebo BMC Cardiovasc Disord Research Myocardial infarction (MI) is a leading cause of mortality. To better understand its molecular and cellular mechanisms, we used bioinformatic tools and molecular experiments to explore the pathogenesis and prognostic markers. Differential gene expression analysis was conducted using GSE60993 and GSE66360 datasets. Hub genes were identified through pathway enrichment analysis and PPI network construction, and four hub genes (AQP9, MMP9, FPR1, and TREM1) were evaluated for their predictive performance using AUC and qRT-PCR. miR-206 was identified as a potential regulator of TREM1. Finally, miR-206 was found to induce EC senescence and ER stress through upregulating mitochondrial ROS levels via TREM1. These findings may contribute to understanding the pathogenesis of MI and identifying potential prognostic markers. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12872-023-03481-8. BioMed Central 2023-09-20 /pmc/articles/PMC10512505/ /pubmed/37730550 http://dx.doi.org/10.1186/s12872-023-03481-8 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Lin, Hao
Chu, Jiapeng
Yuan, Deqiang
Wang, Kangwei
Chen, Fei
Liu, Xuebo
MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1
title MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1
title_full MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1
title_fullStr MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1
title_full_unstemmed MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1
title_short MiR-206 may regulate mitochondrial ROS contribute to the progression of Myocardial infarction via TREM1
title_sort mir-206 may regulate mitochondrial ros contribute to the progression of myocardial infarction via trem1
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10512505/
https://www.ncbi.nlm.nih.gov/pubmed/37730550
http://dx.doi.org/10.1186/s12872-023-03481-8
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