دورية أكاديمية

HAX-1 interferes in assembly of NLRP3-ASC to block microglial pyroptosis in cerebral I/R injury

التفاصيل البيبلوغرافية
العنوان: HAX-1 interferes in assembly of NLRP3-ASC to block microglial pyroptosis in cerebral I/R injury
المؤلفون: Xin-bin Guo, Xin Deng, Jingjing Wang, Yuruo Qi, Wen Zhao, Sheng Guan
المصدر: Cell Death Discovery, Vol 10, Iss 1, Pp 1-13 (2024)
بيانات النشر: Nature Publishing Group, 2024.
سنة النشر: 2024
المجموعة: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
LCC:Cytology
مصطلحات موضوعية: Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671
الوصف: Abstract Acute cerebral ischemia has a high rate of disability and death. Although timely recanalization therapy may rescue the ischemic brain tissue, cerebral ischemia-reperfusion injury has been shown to limit the therapeutic effects of vascular recanalization. Protein HAX-1 has been reported as a pro-survival protein that plays an important role in various disorders, particularly in association with the nervous system. However, the effects and mechanisms of HAX-1 in cerebral IR injury have yet to be elucidated. So, we aimed to investigate the effect of HAX-1 on microglial pyroptosis and explore its potential neuroprotective effects in ischemia-reperfusion injury. Our results show that the expression of HAX-1 decreased after cerebral IR injury, accompanied by an increase in pyroptosis pathway activation. In addition, HAX-1 could inhibit microglial pyroptosis both in vivo and in vitro and reduce the release of inflammatory mediators. The above neuroprotective effects might be partially mediated by inhibiting of interaction of NLRP3 and ASC through competitive binding, followed by the attenuation of NLRP3 inflammasome formation. In conclusion, Our findings support that HAX-1 exhibits a protective role in cerebral I/R injury, and further study on HAX-1 expression regulation will contribute to cerebral infarction therapy.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 2058-7716
Relation: https://doaj.org/toc/2058-7716
DOI: 10.1038/s41420-024-02005-3
URL الوصول: https://doaj.org/article/7e86fd5671354b56a1b4a24e9d7a9387
رقم الأكسشن: edsdoj.7e86fd5671354b56a1b4a24e9d7a9387
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:20587716
DOI:10.1038/s41420-024-02005-3