炎症
医学
冲程(发动机)
脑损伤
神经科学
血脑屏障
脑缺血
缺血
内科学
病理
小胶质细胞
免疫学
中枢神经系统
生物
机械工程
工程类
作者
Kaibin Shi,De‐Cai Tian,Zhiguo Li,Andrew F. Ducruet,Michael T. Lawton,Fu‐Dong Shi
标识
DOI:10.1016/s1474-4422(19)30078-x
摘要
Stroke, including acute ischaemic stroke and intracerebral haemorrhage, results in neuronal cell death and the release of factors such as damage-associated molecular patterns (DAMPs) that elicit localised inflammation in the injured brain region. Such focal brain inflammation aggravates secondary brain injury by exacerbating blood–brain barrier damage, microvascular failure, brain oedema, oxidative stress, and by directly inducing neuronal cell death. In addition to inflammation localised to the injured brain region, a growing body of evidence suggests that inflammatory responses after a stroke occur and persist throughout the entire brain. Global brain inflammation might continuously shape the evolving pathology after a stroke and affect the patients' long-term neurological outcome. Future efforts towards understanding the mechanisms governing the emergence of so-called global brain inflammation would facilitate modulation of this inflammation as a potential therapeutic strategy for stroke.
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