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Journal of Physiology

Resumen/Descripción – provisto por la editorial en inglés
The Journal of Physiology publishes full-length research papers and Techniques for Physiology (introduced in 2008), which are short papers aimed at disseminating new techniques for physiological research. Articles solicited by the Editorial Board include Perspectives, Symposium Reports and Topical Reviews, which highlight areas of special physiological interest. CrossTalk articles are short editorial-style invited articles framing a debate between experts in the field on controversial topics. Letters to the Editor and Journal Club articles are also published. All categories of papers are subjected to the same review procedure.
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Disponibilidad
Institución detectada Período Navegá Descargá Solicitá
No detectada desde ene. 1877 / hasta dic. 2023 Wiley Online Library

Información

Tipo de recurso:

revistas

ISSN impreso

0022-3751

ISSN electrónico

1469-7793

País de edición

Estados Unidos

Fecha de publicación

Cobertura temática

Tabla de contenidos

Neuroinflammation and the immune system in hypoxic ischaemic brain injury pathophysiology after cardiac arrest

Mypinder S. SekhonORCID; Sophie Stukas; Veronica Hirsch‐Reinshagen; Sonny Thiara; Tison Schoenthal; Michael Tymko; Kelly M. McNagny; Cheryl Wellington; Ryan HoilandORCID

<jats:title>Abstract</jats:title><jats:p>Hypoxic ischaemic brain injury after resuscitation from cardiac arrest is associated with dismal clinical outcomes. To date, most clinical interventions have been geared towards the restoration of cerebral oxygen delivery after resuscitation; however, outcomes in clinical trials are disappointing. Therefore, alternative disease mechanism(s) are likely to be at play, of which the response of the innate immune system to sterile injured tissue <jats:italic>in vivo</jats:italic> after reperfusion has garnered significant interest. The innate immune system is composed of three pillars: (i) cytokines and signalling molecules; (ii) leucocyte migration and activation; and (iii) the complement cascade. In animal models of hypoxic ischaemic brain injury, pro‐inflammatory cytokines are central to propagation of the response of the innate immune system to cerebral ischaemia–reperfusion. In particular, interleukin‐1 beta and downstream signalling can result in direct neural injury that culminates in cell death, termed pyroptosis. Leucocyte chemotaxis and activation are central to the <jats:italic>in vivo</jats:italic> response to cerebral ischaemia–reperfusion. Both parenchymal microglial activation and possible infiltration of peripherally circulating monocytes might account for exacerbation of an immunopathological response in humans. Finally, activation of the complement cascade intersects with multiple aspects of the innate immune response by facilitating leucocyte activation, further cytokine release and endothelial activation. To date, large studies of immunomodulatory therapies have not been conducted; however, lessons learned from historical studies using therapeutic hypothermia in humans suggest that quelling an immunopathological response might be efficacious. Future work should delineate the precise pathways involved <jats:italic>in vivo</jats:italic> in humans to target specific signalling molecules. <jats:boxed-text content-type="graphic" position="anchor"><jats:graphic xmlns:xlink="http://www.w3.org/1999/xlink" mimetype="image/png" position="anchor" specific-use="enlarged-web-image" xlink:href="graphic/tjp15709-gra-0001-m.png"><jats:alt-text>image</jats:alt-text></jats:graphic></jats:boxed-text></jats:p>

Palabras clave: Physiology.

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