The Role of Fibrinogen and Platelets in Mouse Liver Ischemia-Reperfusion Injury: Distribution and Pathophysiological Insights.

Abstract

Liver ischemia-reperfusion (I/R) injury is a critical issue in clinical settings, particularly in liver transplantation and resection, leading to severe hepatocellular dysfunction and organ failure. This study investigates the role of fibrinogen and platelets in liver I/R injury, focusing on their distribution and pathophysiological impact within liver lobules. Using a mouse model, we examined the expression and localization of fibrinogen and platelets at various time points postreperfusion. In normal liver, fibrinogen is predominantly expressed in hepatic sinusoids near the portal vein, with sparse platelet distribution. Following I/R injury, fibrinogen expression significantly increases in hepatic sinusoids and hepatocytes, accompanied by substantial platelet aggregation and embolization, particularly in Zone 1 of the liver lobules. These findings highlight the zonal heterogeneity of fibrinogen distribution and its regulatory function in platelet adhesion and microthrombi formation. This study provides crucial insights for developing therapeutic strategies targeting fibrinogen and platelet interactions to mitigate liver I/R injury.