MiRNA: Involvement of the MAPK Pathway in Ischemic Stroke. A Promising Therapeutic Target
Ischemic stroke (IS) is a cerebrovascular disease with a high rate of disability and mortality. It is classified as the second leading cause of death that arises from the sudden occlusion of small vessels in the brain with consequent lack of oxygen and nutrients in the brain tissue. Following an acu...
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MDPI AG
2021-10-01
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author | Agnese Gugliandolo Serena Silvestro Cinzia Sindona Placido Bramanti Emanuela Mazzon |
author_facet | Agnese Gugliandolo Serena Silvestro Cinzia Sindona Placido Bramanti Emanuela Mazzon |
author_sort | Agnese Gugliandolo |
collection | DOAJ |
description | Ischemic stroke (IS) is a cerebrovascular disease with a high rate of disability and mortality. It is classified as the second leading cause of death that arises from the sudden occlusion of small vessels in the brain with consequent lack of oxygen and nutrients in the brain tissue. Following an acute ischemic event, the cascade of events promotes the activation of multiple signaling pathways responsible for irreversible neuronal damage. The mitogen-activated protein kinase (MAPK) signaling pathway transmits signals from the cell membrane to the nucleus in response to different stimuli, regulating proliferation, differentiation, inflammation, and apoptosis. Several lines of evidence showed that MAPK is an important regulator of ischemic and hemorrhagic cerebral vascular disease; indeed, it can impair blood–brain barrier (BBB) integrity and exacerbate neuroinflammation through the release of pro-inflammatory mediators implementing neurovascular damage after ischemic stroke. This review aims to illustrate the miRNAs involved in the regulation of MAPK in IS, in order to highlight possible targets for potential neuroprotective treatments. We also discuss some miRNAs (miR), including miR-145, miR-137, miR-493, and miR-126, that are important as they modulate processes such as apoptosis, neuroinflammation, neurogenesis, and angiogenesis through the regulation of the MAPK pathway in cerebral IS. To date, limited drug therapies are available for the treatment of IS; therefore, it is necessary to implement preclinical and clinical studies aimed at discovering novel therapeutic approaches to minimize post-stroke neurological damage. |
first_indexed | 2024-03-10T06:25:11Z |
format | Article |
id | doaj.art-b047f920bee54194af46eb36c12bec07 |
institution | Directory Open Access Journal |
issn | 1010-660X 1648-9144 |
language | English |
last_indexed | 2024-03-10T06:25:11Z |
publishDate | 2021-10-01 |
publisher | MDPI AG |
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spelling | doaj.art-b047f920bee54194af46eb36c12bec072023-11-22T19:04:07ZengMDPI AGMedicina1010-660X1648-91442021-10-015710105310.3390/medicina57101053MiRNA: Involvement of the MAPK Pathway in Ischemic Stroke. A Promising Therapeutic TargetAgnese Gugliandolo0Serena Silvestro1Cinzia Sindona2Placido Bramanti3Emanuela Mazzon4IRCCS Centro Neurolesi “Bonino-Pulejo”, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, ItalyIRCCS Centro Neurolesi “Bonino-Pulejo”, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, ItalyIRCCS Centro Neurolesi “Bonino-Pulejo”, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, ItalyIRCCS Centro Neurolesi “Bonino-Pulejo”, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, ItalyIRCCS Centro Neurolesi “Bonino-Pulejo”, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, ItalyIschemic stroke (IS) is a cerebrovascular disease with a high rate of disability and mortality. It is classified as the second leading cause of death that arises from the sudden occlusion of small vessels in the brain with consequent lack of oxygen and nutrients in the brain tissue. Following an acute ischemic event, the cascade of events promotes the activation of multiple signaling pathways responsible for irreversible neuronal damage. The mitogen-activated protein kinase (MAPK) signaling pathway transmits signals from the cell membrane to the nucleus in response to different stimuli, regulating proliferation, differentiation, inflammation, and apoptosis. Several lines of evidence showed that MAPK is an important regulator of ischemic and hemorrhagic cerebral vascular disease; indeed, it can impair blood–brain barrier (BBB) integrity and exacerbate neuroinflammation through the release of pro-inflammatory mediators implementing neurovascular damage after ischemic stroke. This review aims to illustrate the miRNAs involved in the regulation of MAPK in IS, in order to highlight possible targets for potential neuroprotective treatments. We also discuss some miRNAs (miR), including miR-145, miR-137, miR-493, and miR-126, that are important as they modulate processes such as apoptosis, neuroinflammation, neurogenesis, and angiogenesis through the regulation of the MAPK pathway in cerebral IS. To date, limited drug therapies are available for the treatment of IS; therefore, it is necessary to implement preclinical and clinical studies aimed at discovering novel therapeutic approaches to minimize post-stroke neurological damage.https://www.mdpi.com/1648-9144/57/10/1053ischemic strokemiRNAMAPK pathway |
spellingShingle | Agnese Gugliandolo Serena Silvestro Cinzia Sindona Placido Bramanti Emanuela Mazzon MiRNA: Involvement of the MAPK Pathway in Ischemic Stroke. A Promising Therapeutic Target Medicina ischemic stroke miRNA MAPK pathway |
title | MiRNA: Involvement of the MAPK Pathway in Ischemic Stroke. A Promising Therapeutic Target |
title_full | MiRNA: Involvement of the MAPK Pathway in Ischemic Stroke. A Promising Therapeutic Target |
title_fullStr | MiRNA: Involvement of the MAPK Pathway in Ischemic Stroke. A Promising Therapeutic Target |
title_full_unstemmed | MiRNA: Involvement of the MAPK Pathway in Ischemic Stroke. A Promising Therapeutic Target |
title_short | MiRNA: Involvement of the MAPK Pathway in Ischemic Stroke. A Promising Therapeutic Target |
title_sort | mirna involvement of the mapk pathway in ischemic stroke a promising therapeutic target |
topic | ischemic stroke miRNA MAPK pathway |
url | https://www.mdpi.com/1648-9144/57/10/1053 |
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