Carvedilol decreases hepatic vascular resistance by reducing fibrogenesis and reversing endothelial dysfunction in cirrhotic rats

Carvedilol is considered the best β-blocker for treating portal hypertension. In this study we show that carvedilol, unlike traditional β-blockers such as propranolol, downregulates the factors that lead to increased portal pressure in cirrhosis: it lowers the hepatic vascular tone by counteracting hepatic sinusoidal endothelial dysfunction, and decreases liver fibrosis by deactivating hepatic stellate cells and inhibiting their proliferation. On top of decreasing portal vein inflow via its non-selective β-blocker effect. Moreover, through its antioxidant and anti-inflammatory activity, it may contribute to improving liver function. These effects are noted both in early and in advanced cirrhosis, suggesting that it can be effective in slowing/reversing disease progression when associated with etiological therapy.

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Publication Details

Journal
JHEP Reports
Published
2025-11-21
DOI
https://doi.org/10.1016/j.jhepr.2025.101681
Primary Topic
Liver Disease and Transplantation
Type
article
Field-Weighted Citation Impact
0.00

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article

Carvedilol decreases hepatic vascular resistance by reducing fibrogenesis and reversing endothelial dysfunction in cirrhotic rats

Jaime Bosch, Éric Felli, Jordi Gracia‐Sancho, Annalisa Berzigotti et al.
JHEP Reports
Liver Disease and Transplantation
article

Carvedilol decreases hepatic vascular resistance by reducing fibrogenesis and reversing endothelial dysfunction in cirrhotic rats

Jaime Bosch, Éric Felli, Jordi Gracia‐Sancho, Annalisa Berzigotti, Sonia Selicean, Yeldos Nulan, Manuel Prampolini
article en

Abstract

Carvedilol is considered the best β-blocker for treating portal hypertension. In this study we show that carvedilol, unlike traditional β-blockers such as propranolol, downregulates the factors that lead to increased portal pressure in cirrhosis: it lowers the hepatic vascular tone by counteracting hepatic sinusoidal endothelial dysfunction, and decreases liver fibrosis by deactivating hepatic stellate cells and inhibiting their proliferation. On top of decreasing portal vein inflow via its non-selective β-blocker effect. Moreover, through its antioxidant and anti-inflammatory activity, it may contribute to improving liver function. These effects are noted both in early and in advanced cirrhosis, suggesting that it can be effective in slowing/reversing disease progression when associated with etiological therapy.

JHEP ReportsVol. 8(3)
University of Bern (CH), University Hospital of Bern (CH), Institut d'Investigacions Biomèdiques de Barcelona (ES)
University of Bern, Inselspital, Universitätsspital Bern
Openalex Percentile: Top 54%
Liver Disease and Transplantation
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