From Liver Fibrosis to Hepatocarcinogenesis: Role of Excessive Liver HO and Targeting Nanotherapeutics

Overview

Journal Bioact Mater

Specialty Biomedical Engineering

Date 2022 Nov 21

PMID 36406254

Authors

Meiyu Shao

Yifan Wang

Hongyan Dong

Lu Wang

Xiaoqing Zhang

Xin Han

Xianan Sang

Yini Bao

Mengyun Peng

Gang Cao

Affiliations

Soon will be listed here.

Abstract

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 HO 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. HO accumulation is associated with overproduction of superoxide anion (O ) and abolished antioxidant enzyme systems. Plenty of therapeutics focused on HO have shown satisfactory effects against liver fibrosis or HCC in different ways. This review summarized the reasons of liver HO accumulation, and the role of HO in genesis of liver fibrosis and HCC. Additionally, nanotherapeutics targeting HO were summarized for further consideration of antifibrotic or antitumor therapy.

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