Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation; Cells; Vol. 9, iss. 11

Alarmins and c-Jun N-Terminal Kinase (JNK) Signaling in Neuroinflammation; Cells; Vol. 9, iss. 11

書誌詳細
Parent link:Cells
Vol. 9, iss. 11.— 2020.— [2350, 26 p.]
団体著者: Национальный исследовательский Томский политехнический университет Инженерная школа новых производственных технологий Научно-образовательный центр Н. М. Кижнера
その他の著者: Anfinogenova Ya. J. Yana Jonovna, Quinn M. T. Mark, Schepetkin (Shchepyotkin) I. A. Igor Aleksandrovich, Atochin D. N. Dmitry Nikolaevich
要約:Title screen
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.
言語:英語
出版事項: 2020
主題:
электронный ресурс
труды учёных ТПУ
alarmin
neuroinflammation
Alzheimer's disease
microglia
c-Jun N-terminal kinase
high-mobility group box protein 1
BAG family molecular chaperone regulator 3
オンライン･アクセス:https://doi.org/10.3390/cells9112350
フォーマット: 電子媒体 図書の章
KOHA link:https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=663500

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