Figures 6 and 7 show      mitochondria (the powerhouse of the cell) responding to model stroke and      sovateltide. Are mitochondria only important because of their critical      role in energy homeostasis? If not (obviously the answer to that last      question is “no”), what are some consequences of mitochondrial      dysfunction following ischemia/reperfusion? That is, what’s the mechanism      by which damage to the mitochondria causes/worsens the lesion in the brain