Liver fibrosis is a major global health problem due to its increasing prevalence and lack of effective therapeutic approaches.  

Recently, researchers from the Universitat de València and the CIBERehd (Liver and Digestive Diseases Networking Biomedical Research Centre) have described how the antiretroviral drug Rilpivirine (RPV), already marketed and used in the treatment of HIV infection, is able to reduce liver fibrosis in different pre-clinical models of liver damage.

The results obtained and published in the journal Gut highlight the need to find selective therapies to efficiently treat patients with fibrosis, intervening on the inactivation of stellate cells and regeneration of liver tissue.

Coordinated by Ana Blas-García (Universitat de València-CIBERehd), and the first author of the article, Alberto Martí-Rodrigo, from the Digestive Pharmacology and Inflammation Research Unit from the Faculty of Medicine and Dentistry of this university, the work has been carried out with the collaboration of the group of Hepatic Vascular Biology of IDIBAPS-CIBERehd (Barcelona).

The study shows that VRP inhibits lipid accumulation and has anti-inflammatory and anti-fibrotic effects in preclinical models of chronic liver disease, regardless of their aetiology, which is of great clinical relevance since liver fibrosis represents a factor common to all chronic liver diseases.

The protective effect of this drug has been confirmed in a retrospective study analysing clinical data from public databases of HIV-infected patients treated with different antiretroviral guidelines, where it is observed that patients treated with this drug have better liver function.

The actions described in this paper could represent an effective strategy for the treatment of liver diseases with fibrotic component and could help to identify new therapeutic targets.

Reference:

Rilpivirineattenuates liver fibrosis through selective STAT1-mediated apoptosis in hepatic stellate cells.

Gut.  2019 Sep 17. pii: gutjnl-2019-318372. doi: 10.1136/gutjnl-2019-318372.