AI Article Synopsis
- Liver fibrosis can be reversed in its early stages, but if it progresses to cirrhosis, it poses a significant risk for developing hepatocellular carcinoma (HCC).
- Excessive accumulation of heme oxygenase (HO) in pathologically affected livers negatively affects liver cell functionality and contributes to the development of fibrosis and HCC.
- The review discusses various causes of HO accumulation, its role in liver disease progression, and highlights emerging nanotherapeutics that target HO for potential antifibrotic and antitumor treatments.
Article 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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9663332 | PMC |
| http://dx.doi.org/10.1016/j.bioactmat.2022.11.001 | DOI Listing |
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