Stroke is the leading cause of death and the main cause of disability in surviving patients. The detrimental interaction between immune cells, glial cells, and matrix components in stroke pathology results in persistent inflammation that progresses to fibrosis. A substantial effort is being directed toward understanding the exact neuroinflammatory events that take place as a result of stroke. The initiation of a potent cytokine response, along with immune cell activation and infiltration in the ischemic core, has massive acute deleterious effects, generally exacerbated by comorbid inflammatory conditions. There is secondary neuroinflammation that promotes further injury, resulting in cell death, but conversely plays a beneficial role, by promoting recovery. This highlights the need for a better understanding of the neuroinflammatory and fibrotic processes, as well as the need to identify new mechanisms and potential modulators. In this review, we summarize several aspects of stroke-induced inflammation, fibrosis, and include a discussion of cytokine inhibitors/inducers, immune cells, and fibro-inflammation signaling inhibitors in order to identify new pharmacological means of intervention.

中文翻译：

---

中风中的神经炎症和纤维化：好的、坏的和丑陋的


中风是死亡的主要原因，也是幸存患者残疾的主要原因。在中风病理学中，免疫细胞、神经胶质细胞和基质成分之间的有害相互作用导致持续性炎症，进而进展为纤维化。人们正在努力了解中风导致的确切神经炎症事件。强效细胞因子反应的启动，以及缺血核心的免疫细胞激活和浸润，具有巨大的急性有害作用，通常会因共病炎症状况而加剧。继发性神经炎症会促进进一步损伤，导致细胞死亡，但相反，通过促进恢复发挥有益作用。这突出表明需要更好地了解神经炎症和纤维化过程，以及需要确定新的机制和潜在的调节剂。在这篇综述中，我们总结了中风引起的炎症、纤维化的几个方面，并讨论了细胞因子抑制剂/诱导剂、免疫细胞和纤维炎症信号抑制剂，以确定新的药理学干预手段。