In cerebral ischemia, the low-glucose state activates the SENP1-Sirt3 signaling pathway through nonclassical AMPK signaling [49], while the accumulation of glucose intermediate metabolites due to mitochondrial dysfunction, on the other hand, inhibits the classical cytoprotective signaling pathway AMPK-SENP1-Sirt3 (Figure 3). This evidence concerns the gene SENP1 and brain ischemia.