Abstract

Passive hepatic congestion, known as congestive hepatopathy, occurs due to hepatic outflow obstruction, a condition most commonly observed in congestive heart failure. Chronic hepatic congestion can eventually result in hepatic fibrosis. Liver specimens of patients with hepatic congestion are histologically characterized by sinusoidal engorgement and hemorrhagic necrosis in the perivenular areas of the hepatic acini, which leads to sinusoidal fibrosis and ultimately to bridging fibrosis between adjacent central veins.1–2 Our understanding of fibrogenesis in congestive hepatopathy has largely come from pathological examinations of human samples. The mechanisms have remained unclear partly due to the lack of appropriate experimental models.

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