Post-cardiac arrest syndrome (PCAS) is a critical systemic injury caused by ischemia and reperfusion after return of spontaneous circulation in patients after cardiac arrest. It involves multiple organ dysfunctions with complex pathophysiological mechanisms that are not fully understood. Despite advances in clinical management, high rates of morbidity and mortality persist. Current basic research focuses on cellular and molecular changes such as oxidative stress, mitochondrial dysfunction and systemic inflammatory responses. Animal models help mimic the human condition in the search for biomarkers and therapeutic targets. The review summarizes advances in pathophysiology, molecular signaling pathways, and experimental interventions. The aim is to provide a theoretical basis for future translational research and improvement of clinical outcomes.