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Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation

1
Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk 634012, Russia
2
Department of Microbiology and Immunology, Montana State University, Bozeman, MT 59717, USA
3
Kizhner Research Center, Tomsk Polytechnic University, 634050 Tomsk, Russia
4
Cardiovascular Research Center, Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
*
Author to whom correspondence should be addressed.
Cells 2020, 9(11), 2350; https://doi.org/10.3390/cells9112350
Received: 25 August 2020 / Revised: 8 October 2020 / Accepted: 21 October 2020 / Published: 24 October 2020
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. View Full-Text
Keywords: alarmin; neuroinflammation; Alzheimer’s disease; microglia; c-Jun N-terminal kinase; high-mobility group box protein 1; BAG family molecular chaperone regulator 3 alarmin; neuroinflammation; Alzheimer’s disease; microglia; c-Jun N-terminal kinase; high-mobility group box protein 1; BAG family molecular chaperone regulator 3
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MDPI and ACS Style

Anfinogenova, N.D.; Quinn, M.T.; Schepetkin, I.A.; Atochin, D.N. Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation. Cells 2020, 9, 2350.

AMA Style

Anfinogenova ND, Quinn MT, Schepetkin IA, Atochin DN. Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation. Cells. 2020; 9(11):2350.

Chicago/Turabian Style

Anfinogenova, Nina D.; Quinn, Mark T.; Schepetkin, Igor A.; Atochin, Dmitriy N. 2020. "Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation" Cells 9, no. 11: 2350.

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