The role of ubiquitylation in cerebral ischemia-reperfusion injury to reduce mitochondrial dysfunction and programmed...

The morbidity and mortality of cardiac arrest are notably high and a major public health issue worldwide. Cerebral ischemia-reperfusion injury (CIRI) is a major cause of mortality and poor neurological outcome in cardiac arrest patients. Mitochondria, the energy centers of most eukaryotic cells, are a "hub" in CIRI development, and regulating mitochondrial dynamics and mitophagy to maintain the relative quantity and quality of mitochondria in the internal environment has gained attention. Modulating key protein expression in the pyroptosis and ferroptosis pathways is an important strategy in treating CIRI. Ubiquitination, a posttranslational modification, is involved in fundamental pathophysiological processes such as neurological disorders, ischemia-reperfusion injury and inflammation, and oxidative stress. This narrative review summarizes the research progress in ubiquitin protease system intervention affecting mitochondrial homeostasis, pyroptosis, and ferroptosis in the context of CIRI. Our aim is to provide a favorable reference for effectively improving the prognosis of patients with cardiac arrest.