Conclusion
Multiple modes of action are implicated in the etiology of SAH, making it a difficult disease to understand. SAH-induced inflammation appears to be a complicated process. There have been numerous inflammatory pathways explored in SAH, with varying degrees of evidence to support each one. SAH-induced inflammation is mostly controlled by TLR, as described in the above processes and pathways. Antioxidants and TLR inhibitors that target these mediators may not only prevent the activation of downstream inflammatory pathways, but may also improve the prognosis for SAH patients. However, because to the intricacy of SAH, inflammation may not be the only aspect to consider; other events may either enhance or aggravate the symptoms after SAH. There have been several recent studies suggesting that inflammation is the most essential factor to consider in the prevention and treatment of issues that may arise after SAH, such as EBI. Recently, new studies have revealed how TREM-1 inhibition could improve the prognosis of EBI as a secondary brain injury after SAH. Thus more investigations should be carried in the mechanism of TREM-1. Despite the fact that inflammatory pathways offer a wide range of potential targets, further study is needed to determine the importance of these pathways in SAH. To assess the clinical relevance of this discovery, additional clinical trials will be required in the near future.
Acknowledgement: This study was funded by Shanxi Province’s Great Research Project (201903D321044) and Shanxi Health Committee’s Project (2019045).
Conflict of interest: The authors declare that they have no conflict of interest.
Authors’ contributions: All authors were involved in writing the review.
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