Endothelial GATAD1 Exacerbates Blood-brain Barrier Dysfunction in Ischemic Stroke through Caveolae-mediated Transcytosis by Lizhen Fan & Hui Liu & Shanshan Li & Lingling Li & Zhi Zhang & Pinyi Liu & Haiyan Yang & Shengnan Xia & Xiang Cao & Chun Wang & Yun Xu instant download

Endothelial GATAD1 Exacerbates Blood-brain Barrier Dysfunction in Ischemic Stroke through Caveolae-mediated Transcytosis by Lizhen Fan & Hui Liu & Shanshan Li & Lingling Li & Zhi Zhang & Pinyi Liu & Haiyan Yang & Shengnan Xia & Xiang Cao & Chun Wang & Yun Xu instant download

Neuroscience Bulletin,Abstract Blood-brain barrier (BBB) dysfunction repreGATAD1 as a novel regulator of BBB permeability and a sents a critical pathological manifestation in exacerbating potential therapeutic target for ischemic stroke intervention.ischemic stroke, contributing to neuronal death, edema formation, and unfavorable clinical outcomes. GATA zinc Keywords GATAD1 · Blood-brain barrier · fnger domain-containing 1 (GATAD1) is recognized as a Transcytosis · Ischemic strokecritical transcription factor in cardiac development and cardiovascular disease. However, the role of GATAD1 in regulating BBB function and ischemic stroke remains elusive. IntroductionHere, we found that GATAD1 was upregulated in cerebral endothelial cells (ECs) following ischemic stroke in mice. Stroke has been a great challenge, ranking as the third-leading EC-specifc Gatad1 defciency demonstrated remarkable cause of death and disability in recent years globally, in which neuroprotection, manifested by reduced infarct volumes, ischemic stroke contributed 62.4% followed by a growing ecoameliorated BBB dysfunction, and improved neurological nomic and social burden [1]. Although neuronal death constioutcomes following experimental stroke. Mechanistic investutes the primary pathological driver of stroke-related mortigations revealed that GATAD1 was involved in regulating bidity [2], clinical trials targeting neuronal survival pathways CD36 expression, thereby modulating caveolae-mediated have consistently failed, indicating the urgent need for alternatranscytosis in cerebral ECs. These fndings established tive therapeutic approaches focusing on non-neuronal pathophysiology. Emerging evidence positions blood-brain barrier (BBB) dysfunction as a critical early event in ischemic stroke Supplementary Information The online version contains pathogenesis and a promising therapeutic target [3]. The BBB consists of a selectively permeable membrane that features supplem…