Potential enhancement of post-stroke angiogenic response by targeting the oligomeric aggregation of p53 protein

Tumor suppressor gene p53 and its aggregate have been found to be involved in many angiogenesis-related pathways. We explored the possible aggregation formation mechanisms commonly occur after ischemic stroke, such as hypoxia presence of reactive oxygen species (ROS). The angiogenic pathways involving mainly nucleus or cytoplasm, with one exception that occurs mitochondria. Considering high mitochondrial density brain endothelial cells, we proposed cyclophilin D (CypD)-dependent vascular cell (VECs) necrosis pathway occurring mitochondria is major factors affects angiogenesis. Hence, targeting aggregation, a key intermediate pathway, could an alternative therapeutic target for post-stroke management.