Endothelial NMMHC IIA Dissociation From PAR1 Activates the CREB3/ARF4 Signaling in Thrombin-Mediated Intracerebral Hemorrhage

    November 2024 in “ Journal of Advanced Research
    Yujie Dai, Lei Bao, Juan Huang, Miling Zhang, Xiaohong Yu, Yuanyuan Zhang, Fang Li, Boyang Yu, Shuaishuai Gong, Junping Kou
    Studysummary In this study, the researchers reported that NMMHC IIA dissociates from PAR1 and activates the CREB3/ARF4 pathway, worsening thrombin-induced blood-brain barrier damage, suggesting it as a potential therapeutic target for blood-brain barrier-related diseases. Our plain-language summary of this paper — not a Tressless recommendation.
    The study found that the dissociation of NMMHC IIA from PAR1 activates the CREB3/ARF4 signaling pathway, which exacerbates blood-brain barrier (BBB) damage caused by thrombin. This discovery suggests that NMMHC IIA could be a new therapeutic target for treating diseases related to BBB damage.
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