Fig. 3: The transition of the liver microenvironment contributes to HCC development. | Experimental & Molecular Medicine

Fig. 3: The transition of the liver microenvironment contributes to HCC development.

From: Protein phosphatases regulate the liver microenvironment in the development of hepatocellular carcinoma

Fig. 3

Stimulation by liver injury/damage can induce Kupffer cells to produce proinflammatory cytokines and TGF-β. The migration of immune cells is induced by the proinflammatory response. The proinflammatory immune response can increase Th17 cell differentiation. TGF-β can promote the activation of HSCs, contributing to collagen fiber production and the development of hepatic cirrhosis. In hepatic cirrhosis, the anti-inflammatory response is increased. Increasing Th2 cell differentiation can induce the M2-like transition of macrophages. Activated HSCs can induce the development of MDSCs as well as immature DCs. Increased TGF-β can induce EMT in hepatocytes. Chronic liver inflammation can induce the dedifferentiation of hepatocytes. Hypoxia caused by hepatic cirrhosis and angiogenesis can constitute the protumoral liver microenvironment.

Back to article page