Sepsis is a life-threatening organ dysfunction syndrome caused by dysregulation of the host's response to infection, characterized by high morbidity and mortality. The liver is a key metabolic and immune organ in the progression of sepsis, and sepsis-associated liver injury (SALI) is an independent predictor of mortality in sepsis patients. Hepatic dysfunction can severely impair their prognosis, and alleviating SALI is crucial for reducing the mortality of sepsis patients. The pathogenesis of SALI is complex, and pyroptosis, as a pro-inflammatory form of programmed cell death, plays a key role in it. Pyroptosis is regulated through classical (NLRP3-caspase-1-GSDMD) and non-classical (caspase-4/5/11-GSDMD) pathways. The pyroptosis of different cell types in the liver, such as hepatocytes, hepatic macrophages, and neutrophils, can participate in the process of SALI through mechanisms such as inflammation amplification and microcirculatory disturbance. At present, some existing hepatoprotective drugs in clinical practice have been proven to have anti-pyroptotic effects. Some natural compounds, synthetic drugs, endogenous active molecules, and stem cell therapy can also alleviate SALI by regulating pyroptosis pathways. In conclusion, pyroptosis is a key mechanism of SALI, and in-depth exploration of its regulatory mechanisms and intervention drugs can provide new strategies for the precise prevention and treatment of SALI.