Abstract
The pathogenesis of ischemia-reperfusion injury is not fully understood, most of the current clinical treatment methods mainly relieve symptoms, and cannot prevent fundamentally. The mechanism of Ferroptosis has been extensively studied in recent years, but primarily focused on its therapeutic effects on tumors. After careful comparison, it is easy to find that the symptoms of ischemia-reperfusion injury often accompany by increased lipid peroxidation and increased intracellular iron level are the same as the manifestations of iron-dependent non-apoptotic Ferroptosis. Based on this "coincidence", we launched this survey. After reading a lot of literature, we found that Ferroptosis is the first step of ischemia-reperfusion injury, and cell necrosis and inflammation are the subsequent steps secondary to Ferroptosis. In this review, we have collected and sorted out the current knowledge about the role and targets of Ferroptosis in the process of ischemia-reperfusion injury. And future studies may be biased towards exploring the use of ferroptosis inhibitors in combination with other treatment options.