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Hepatotoxicity is damage or injury to the liver as a result of damaging or destructive agents such as drugs or industrial chemicals which are termed hepatotoxins.
The redox status of a cell is regulated through a number of mechanisms, chief among these is the KEAP1-mediated ubiquitination and degradation of NRF2. Here the authors show that KEAP1 itself is ubiquitinated and degraded in a process that is opposed by the ubiquitin-specific protease USP25.
A prospective study suggests that the risk of liver fibrosis with methotrexate treatment has been overestimated. The findings suggest the need to reconsider the intensive strategies and the screening tools that are recommended for monitoring liver fibrosis in patients receiving methotrexate.
In an adult mouse model of tyrosinaemia, a base editor correcting an A-to-G splice-site mutation in the Fah gene restores the translation of the functional enzyme, promoting the repopulation of the liver with the corrected cells.
