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Mechanism of Pyroptosis in Acute Liver Injury and Prospect of Targeted Therapy
Summary
This review examined the role of pyroptosis—an inflammatory form of programmed cell death—in acute liver injury, covering the gasdermin-mediated molecular mechanisms involved. The authors proposed that targeting pyroptosis pathways may offer new therapeutic strategies for conditions such as drug-induced liver injury and ischemia-reperfusion damage.
Acute liver injury is a critical clinical syndrome characterized by rapid necrosis of hepatocytes and severe inflammatory reaction. At present, effective treatments for its fundamental pathogenic connections are lacking. In recent years, studies have found that pyroptosis, as a programmed inflammatory cell death mode mediated by gasdermin protein, plays a central role in the occurrence and development of a variety of acute liver injury. In this process, the inflammasome senses danger signals and activates caspase-1, which in turn cleaves GSDMD protein and forms cell membrane pores, ultimately leading to cell osmotic lysis and the release of a large number of pro-inflammatory factors. This article systematically elaborated the specific activation pathways and mechanisms of pyroptosis in different types of liver injury, such as drug-induced liver injury, ischemia-reperfusion injury, viral / autoimmune hepatitis and sepsis, and discussed the therapeutic prospect of targeted intervention on the key nodes of pyroptosis. Despite the challenges of crosstalk coexistence of cell death modes and safety of targeted therapy, the development of specific GSDMD inhibitors, analysis of cell heterogeneity using single-cell technology, and exploration of combination treatment strategies still bring new hope to this field. A thorough understanding of pyroptosis mechanism will provide crucial theoretical underpinnings and innovative ideas for the precise prevention and management of acute liver injury.
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