Endothelial NMMHC IIA dissociation from PAR1 activates the CREB3/ARF4 signaling in thrombin-mediated intracerebral hemorrhage
The findings indicated that NMMHC IIA dissociated from PAR1 and activated CREB3/ARF4 pathway, which aggravated BBB damage induced by thrombin. This suggested that NMMHC IIA was a novel potential therapeutic target for BBB-related diseases.
Authors
- Yuanyuan Zhang (ORCID: https://orcid.org/0000-0001-6258-0176)
- Junping Kou (ORCID: https://orcid.org/0000-0001-8377-915X)
- Boyang Yu (ORCID: https://orcid.org/0000-0002-1401-9250)
- Yujie Dai (ORCID: https://orcid.org/0009-0000-6368-5033)
- Miling Zhang
- Xiaohong Yu (ORCID: https://orcid.org/0000-0002-7321-0207)
- Fang Li (ORCID: https://orcid.org/0000-0002-8960-8404)
- Lei Bao (ORCID: https://orcid.org/0000-0002-7834-4327)
- Shuaishuai Gong (ORCID: https://orcid.org/0000-0002-4563-0204)
- Juan Huang (ORCID: https://orcid.org/0000-0002-2643-6684)
Institutions
- China Pharmaceutical University (CN)
Publication Details
- Journal
- Journal of Advanced Research
- Published
- 2024-11-07
- DOI
- https://doi.org/10.1016/j.jare.2024.11.008
- Citations
- 4
- Primary Topic
- Intracerebral and Subarachnoid Hemorrhage Research
- Type
- article
- Field-Weighted Citation Impact
- 1.48
Funders
- National Natural Science Foundation of China
- China Pharmaceutical University
- Government of Jiangsu Province
- Natural Science Foundation of Jiangsu Province