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- W2376892362 abstract "Cardiac arrest (CA) is a leading cause of fatality and long-term disability worldwide. Recent advances in cardiopulmonary resuscitation (CPR) have improved survival rates; however, the survivors are prone to severe neurological injury subsequent to successful CPR following CA. Effective therapeutic options to protect the brain from CA remain limited, due to the complexities of the injury cascades caused by global cerebral ischemia/reperfusion (I/R). Although the precise mechanisms of neurological impairment following CA-initiated I/R injury require further clarification, evidence supports that one of the key cellular pathways of cerebral injury is inflammation. The inflammatory response is orchestrated by activated glial cells in response to I/R injury. Increased release of danger-associated molecular pattern molecules and cellular dysfunction in activated microglia and astrocytes contribute to ischemia-induced cytotoxic and pro-inflammatory cytokines generation, and ultimately to delayed death of neurons. Furthermore, cytokines and adhesion molecules generated within activated microglia, as well as astrocytes, are involved in the innate immune response; modulate influx of peripheral immune and inflammatory cells into the brain, resulting in neurological injury. The present review discusses the molecular aspects of immune and inflammatory mechanisms in global cerebral I/R injury following CA and CPR, and the potential therapeutic strategies that target neuroinflammation and the innate immune system." @default.
- W2376892362 created "2016-06-24" @default.
- W2376892362 creator A5013089507 @default.
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- W2376892362 creator A5068572973 @default.
- W2376892362 creator A5077001895 @default.
- W2376892362 creator A5089370169 @default.
- W2376892362 date "2016-05-16" @default.
- W2376892362 modified "2023-10-11" @default.
- W2376892362 title "Inflammatory mechanisms involved in brain injury following cardiac arrest and cardiopulmonary resuscitation" @default.
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