fig1

Figure 1. AP-1 in chronic liver disease. The AP-1 transcription factor has been described to play a critical role in the pathogenesis and progression of various liver diseases, including precancerous diseases and HCC. This scheme illustrates the different mechanisms modulated by abnormal AP-1 activity, which enhance a context of chronic liver damage, such as MASLD and cirrhosis, preceding the development of HCC. AP-1 is involved in both the damaged hepatocyte and non-parenchymal liver cells through the regulation of gene expression, leading to disease progression. Furthermore, AP-1 promotes the activity mediated by HBV and HCV to eventually favor hepatic pathogenesis. Figure created in Biorender.com. MASLD: Metabolic dysfunction-associated steatotic liver disease; MASH: metabolic dysfunction-associated steatohepatitis; PLC: parenchymal liver cells; NPLC: non-parenchymal liver cells; AP-1: activator protein 1; HCC: hepatocellular carcinoma; HBV: hepatitis B viruses; HCV: hepatitis C viruses; HSCs: hepatic stellate cells; JNK: c-Jun NH2-terminal kinase; TGF-β1: transforming growth factor-β1; IKK: IκB kinase; ER: endoplasmic reticulum; NF-κB: nuclear factor kappa B; MMPs: matrix metallopeptidases; COX-2: cyclooxygenase 2; TIMP1: tissue inhibitor of metalloprotease-1; ROS: reactive oxygen species.