Contrary to our findings, other previous studies reported that Cav-1 mediated tight junction protein Claudin-5 endocytosis and then degradation via autophagy, notably prevented the accumulation of damaged Claudin-5 in the cytoplasm and benefitted cerebral ischemia recovery 37, and in intestinal epithelial barrier inflammatory model, autophagy is necessary to maintain barrier function via inhibiting the loss of tight junction protein Occludin 52. This evidence concerns the gene CLDN5 and brain ischemia.