Publication Summary:

Hepatic fibrosis is an abnormal wound healing response orchestrated by complex intercellular interactions among hepatocytes (HCs), endothelial cells (ECs), hepatic stellate cells (HSCs), Kupffer cells (KCs), and recruited inflammatory cells. The key initiating and series of adaptive events that perpetuate this response, especially in humans, are still not well understood. The recent availability of bioprinted human liver tissue models that incorporate both parenchymal and non-parenchymal cells (NPCs) in a 3D context has created the opportunity to examine progressive liver injury in response to pro-fibrotic modulators and compounds.