Mitochondria as target for antiischemic drugs

The cessation of blood flow followed by a reperfusion period results in severe damages to cell structures. This induces a complex cascade of events involving, more particularly, a loss of energy, an alteration of ionic homeostasis promoting H+ and Ca2+ build up and the generation of free radicals. In this context, mitochondria are highly vulnerable and play a predominant role in the cell signaling leading from life to death. This is why, recently, efforts to find an effective therapy for ischemia–reperfusion injury have focused on mitochondria. This review summarizes the pharmacological strategies which are currently developed and the potential mitochondrial targets which could be involved in the protection of cells.