An-qi Chen

TL;DR: Anti-TNFα (infliximab, a potent clinically used drug) treatment significantly ameliorate endothelial necroptosis, BBB destruction and improve stroke outcomes and suggest infliximab might serve as a potential drug for stroke therapy.

TL;DR: In this paper, the authors highlight the role of circulating and cerebral immune cells in BBB disruption and the crosstalk between them following acute ischemic stroke and discuss potential and effective immunotherapeutic targets to regulate BBB permeability.

TL;DR: This study indicates an alternative therapeutic strategy with anti‐Sema4D to complement or improve the current treatment of DR and found that Sema 4D/PlexinB1 induced endothelial cell dysfunction via mDIA1, which was mediated through Src‐dependent VE‐cadherin dysfunction.

TL;DR: It is found that semaphorin-3A (Sema3A) was significantly downregulated in VSMCs during neointimal hyperplasia after vascular injury in mice and in human atherosclerotic plaques.

TL;DR: This study reveals that Sema3E/PlexinD1 signaling, which suppressed endothelial DLL4 expression, cell motility, and filopodia formation, is expected to be a novel druggable target for angiogenesis during poststroke progression.