Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic target

Background: Globally, myocardial infarction (MI) is one of the main causes of death. This study aims to investigate the role of miR-217 in the pathogenesis through targeting MAPK and PI3K/AKT signaling pathways in experimental model of myocardial infarction and studying the possible cardioprotective...

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Main Authors: Mai A. Zaafan, Amr M. Abdelhamid
Format: Article
Language:English
Published: KeAi Communications Co., Ltd. 2025-02-01
Series:Non-coding RNA Research
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Online Access:http://www.sciencedirect.com/science/article/pii/S2468054024001409
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author Mai A. Zaafan
Amr M. Abdelhamid
author_facet Mai A. Zaafan
Amr M. Abdelhamid
author_sort Mai A. Zaafan
collection DOAJ
description Background: Globally, myocardial infarction (MI) is one of the main causes of death. This study aims to investigate the role of miR-217 in the pathogenesis through targeting MAPK and PI3K/AKT signaling pathways in experimental model of myocardial infarction and studying the possible cardioprotective role of dihydromyricetin (DHM) through modulation of this pathway. Methods: Dihydromyricetin was injected (100 mg/kg; p.o.) in isoprenaline induced myocardial infarction rat model for 14 days. Rats were anaesthetized and blood samples were taken for serum separation, estimation of creatine kinase-MB (CK-MB), and troponin-I levels after 24 h had passed since the last isoprenaline injection. In addition, the hearts were also used for the other biochemical studies and the histological evaluation. Results: DHM resulted in a significant suppression of the elevated levels miR-217 and MAPK compared to the MI control group and restored the normal level of serum CK-MB. Furthermore, DHM successfully restored the oxidative balance and halted the pro-inflammatory mediators in the cardiac tissue. Conclusion: Accordingly, our experiment emphasizes the anti-ischemic property that has been demonstrated through modulation of expression level of miR-217 and consequent deactivation of MAPK and PI3K/AKT signaling pathways, and this was assured by halting downstream pro-inflammatory markers.
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spelling doaj-art-8e628cbf9adc4f39a78f0c549f0305bc2025-08-20T02:47:37ZengKeAi Communications Co., Ltd.Non-coding RNA Research2468-05402025-02-011019219710.1016/j.ncrna.2024.09.007Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic targetMai A. Zaafan0Amr M. Abdelhamid1Pharmacology and Toxicology Department, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), Egypt; Corresponding author.Biochemistry Department, Faculty of Pharmacy, October University for Modern Sciences and Arts (MSA), EgyptBackground: Globally, myocardial infarction (MI) is one of the main causes of death. This study aims to investigate the role of miR-217 in the pathogenesis through targeting MAPK and PI3K/AKT signaling pathways in experimental model of myocardial infarction and studying the possible cardioprotective role of dihydromyricetin (DHM) through modulation of this pathway. Methods: Dihydromyricetin was injected (100 mg/kg; p.o.) in isoprenaline induced myocardial infarction rat model for 14 days. Rats were anaesthetized and blood samples were taken for serum separation, estimation of creatine kinase-MB (CK-MB), and troponin-I levels after 24 h had passed since the last isoprenaline injection. In addition, the hearts were also used for the other biochemical studies and the histological evaluation. Results: DHM resulted in a significant suppression of the elevated levels miR-217 and MAPK compared to the MI control group and restored the normal level of serum CK-MB. Furthermore, DHM successfully restored the oxidative balance and halted the pro-inflammatory mediators in the cardiac tissue. Conclusion: Accordingly, our experiment emphasizes the anti-ischemic property that has been demonstrated through modulation of expression level of miR-217 and consequent deactivation of MAPK and PI3K/AKT signaling pathways, and this was assured by halting downstream pro-inflammatory markers.http://www.sciencedirect.com/science/article/pii/S2468054024001409miRNA-217MAPKPI3KCardioprotectiveDihydromyricetin
spellingShingle Mai A. Zaafan
Amr M. Abdelhamid
Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic target
Non-coding RNA Research
miRNA-217
MAPK
PI3K
Cardioprotective
Dihydromyricetin
title Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic target
title_full Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic target
title_fullStr Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic target
title_full_unstemmed Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic target
title_short Molecular insight of miRNA-217 role in the pathogenesis of myocardial infarction: Promising diagnostic biomarker and therapeutic target
title_sort molecular insight of mirna 217 role in the pathogenesis of myocardial infarction promising diagnostic biomarker and therapeutic target
topic miRNA-217
MAPK
PI3K
Cardioprotective
Dihydromyricetin
url http://www.sciencedirect.com/science/article/pii/S2468054024001409
work_keys_str_mv AT maiazaafan molecularinsightofmirna217roleinthepathogenesisofmyocardialinfarctionpromisingdiagnosticbiomarkerandtherapeutictarget
AT amrmabdelhamid molecularinsightofmirna217roleinthepathogenesisofmyocardialinfarctionpromisingdiagnosticbiomarkerandtherapeutictarget