CLDN5 and ischemic stroke: Our studies used in vitro hypoxia or serum starvation models to mimic the onset of ischemic stroke, and we showed that early hypoxia/starvation could induce autophagy and the redistribution of membranous caveolin-1 (Cav-1) and Claudin-5 into cytosol, and autophagosomes mediate the degradation of cytosolically accumulated Claudin-5, thereby eliminating reactive oxygen species (ROS) and protecting the functional integrity of the endothelial barrier (Yang et al., 2019b, 2020).