Sinusoidal events during fibrosing liver injury

Changes in the subendothelial space of Disse and sinusoid as fibrosis develops in response to liver injury include alterations in both cellular responses and extracellular matrix composition. Stellate cell activation leads to accumulation of scar (fibril-forming) matrix. This in turn contributes to the loss of hepatocyte microvilli and sinusoidal endothelial fenestrae, which result in deterioration of hepatic function. Kupffer cell (macrophage) activation accompanies liver injury and contributes to paracrine activation of stellate cells.