Stroke or brain attack is the third leading cause of death and the leading cause of adult disability worldwide. Unfortunately, besides the tPA, no other treatment is available to limit brain damage. Because of the prevalence and seriousness of this disorder, there is a great need for intervention.
The major goal of our research is to unravel the cellular and molecular mechanisms underlying neuronal injury and recovery following ischemia-reperfusion. Our recent study demonstrates angiogenesis is a plausible therapeutic regimen to combat cerebrovascular diseases. Taken our study for example, ectopically expression of cyclooxygenase-1 (COX-1) augments the level of angiogenic factor PGI2 that subsequently activates Peroxisome Proliferator-Activated Receptor-γ (PPAR-γ) and then reduces inflammation against ischemic stroke. PPAR-γ confers resistance to neuronal apoptosis and cerebral infarction by driving 14-3-3ε transcription. Upregulation of 14-3-3εenhances sequestration of phosphorylated Bad, thereby suppressing apoptosis. PPAR-γ can also inhibit ischemia-induced Bcl-2/Bcl-xl degradation and formation of ROS and ROS-related genes, leading to enhance neuronal survival. As quoted from Louis Pasteur: 「When meditating over a disease, I never think of finding a remedy for it, but instead a means of preventing it\\\\