From liver fibrosis to hepatocarcinogenesis: Role of excessive liver H(2)O(2) and targeting nanotherapeutics

Liver fibrosis and hepatocellular carcinoma (HCC) have been worldwide threats nowadays. Liver fibrosis is reversible in early stages but will develop precancerosis of HCC in cirrhotic stage. In pathological liver, excessive H(2)O(2) is generated and accumulated, which impacts the functionality of hepatocytes, Kupffer cells (KCs) and hepatic stellate cells (HSCs), leading to genesis of fibrosis and HCC. H(2)O(2) accumulation is associated with overproduction of superoxide anion (O(2)(•−)) and abolished antioxidant enzyme systems. Plenty of therapeutics focused on H(2)O(2) have shown satisfactory effects against liver fibrosis or HCC in different ways. This review summarized the reasons of liver H(2)O(2) accumulation, and the role of H(2)O(2) in genesis of liver fibrosis and HCC. Additionally, nanotherapeutics targeting H(2)O(2) were summarized for further consideration of antifibrotic or antitumor therapy.