Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation
Neuroinflammation is involved in the progression or secondary injury of multiple brain conditions, including stroke and neurodegenerative diseases. Alarmins, also known as damage-associated molecular patterns, are released in the presence of neuroinflammation and in the acute phase of ischemia. Defe...
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| Format: | Article |
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MDPI AG
2020-10-01
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| Series: | Cells |
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| Online Access: | https://www.mdpi.com/2073-4409/9/11/2350 |
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| author | Nina D. Anfinogenova Mark T. Quinn Igor A. Schepetkin Dmitriy N. Atochin |
| author_facet | Nina D. Anfinogenova Mark T. Quinn Igor A. Schepetkin Dmitriy N. Atochin |
| author_sort | Nina D. Anfinogenova |
| collection | DOAJ |
| description | Neuroinflammation is involved in the progression or secondary injury of multiple brain conditions, including stroke and neurodegenerative diseases. Alarmins, also known as damage-associated molecular patterns, are released in the presence of neuroinflammation and in the acute phase of ischemia. Defensins, cathelicidin, high-mobility group box protein 1, S100 proteins, heat shock proteins, nucleic acids, histones, nucleosomes, and monosodium urate microcrystals are thought to be alarmins. They are released from damaged or dying cells and activate the innate immune system by interacting with pattern recognition receptors. Being principal sterile inflammation triggering agents, alarmins are considered biomarkers and therapeutic targets. They are recognized by host cells and prime the innate immune system toward cell death and distress. In stroke, alarmins act as mediators initiating the inflammatory response after the release from the cellular components of the infarct core and penumbra. Increased c-Jun N-terminal kinase (JNK) phosphorylation may be involved in the mechanism of stress-induced release of alarmins. Putative crosstalk between the alarmin-associated pathways and JNK signaling seems to be inherently interwoven. This review outlines the role of alarmins/JNK-signaling in cerebral neurovascular inflammation and summarizes the complex response of cells to alarmins. Emerging anti-JNK and anti-alarmin drug treatment strategies are discussed. |
| first_indexed | 2024-03-10T15:21:46Z |
| format | Article |
| id | doaj.art-7656a2fc30ea436b81808b116bf13754 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-03-10T15:21:46Z |
| publishDate | 2020-10-01 |
| publisher | MDPI AG |
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| series | Cells |
| spelling | doaj.art-7656a2fc30ea436b81808b116bf137542023-11-20T18:24:23ZengMDPI AGCells2073-44092020-10-01911235010.3390/cells9112350Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in NeuroinflammationNina D. Anfinogenova0Mark T. Quinn1Igor A. Schepetkin2Dmitriy N. Atochin3Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, RussiaDepartment of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USADepartment of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USAKizhner Research Center, Tomsk Polytechnic University, 634050 Tomsk, RussiaNeuroinflammation is involved in the progression or secondary injury of multiple brain conditions, including stroke and neurodegenerative diseases. Alarmins, also known as damage-associated molecular patterns, are released in the presence of neuroinflammation and in the acute phase of ischemia. Defensins, cathelicidin, high-mobility group box protein 1, S100 proteins, heat shock proteins, nucleic acids, histones, nucleosomes, and monosodium urate microcrystals are thought to be alarmins. They are released from damaged or dying cells and activate the innate immune system by interacting with pattern recognition receptors. Being principal sterile inflammation triggering agents, alarmins are considered biomarkers and therapeutic targets. They are recognized by host cells and prime the innate immune system toward cell death and distress. In stroke, alarmins act as mediators initiating the inflammatory response after the release from the cellular components of the infarct core and penumbra. Increased c-Jun N-terminal kinase (JNK) phosphorylation may be involved in the mechanism of stress-induced release of alarmins. Putative crosstalk between the alarmin-associated pathways and JNK signaling seems to be inherently interwoven. This review outlines the role of alarmins/JNK-signaling in cerebral neurovascular inflammation and summarizes the complex response of cells to alarmins. Emerging anti-JNK and anti-alarmin drug treatment strategies are discussed.https://www.mdpi.com/2073-4409/9/11/2350alarminneuroinflammationAlzheimer’s diseasemicrogliac-Jun N-terminal kinasehigh-mobility group box protein 1 |
| spellingShingle | Nina D. Anfinogenova Mark T. Quinn Igor A. Schepetkin Dmitriy N. Atochin Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation Cells alarmin neuroinflammation Alzheimer’s disease microglia c-Jun N-terminal kinase high-mobility group box protein 1 |
| title | Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation |
| title_full | Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation |
| title_fullStr | Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation |
| title_full_unstemmed | Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation |
| title_short | Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation |
| title_sort | alarmins and c jun n terminal kinase jnk signaling in neuroinflammation |
| topic | alarmin neuroinflammation Alzheimer’s disease microglia c-Jun N-terminal kinase high-mobility group box protein 1 |
| url | https://www.mdpi.com/2073-4409/9/11/2350 |
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