ArticleMolecular medicine reports2019
Carvedilol improves liver cirrhosis in rats by inhibiting hepatic stellate cell activation, proliferation, invasion and collagen synthesis.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Liver-nervous system axis: pathways, dysregulation, and translational perspectives.Journal of neuroinflammation · 2026Review
- Carvedilol triggers ferroptosis in hepatic stellate cells via the ATF4/SAT1 axis promoting spermidine depletion to ameliorate liver fibrosis.Cell death & disease · 2026Article
- Using intra-voxel incoherent motion MRI to dynamically evaluate the attenuating effects of donafenib combined with carvedilol in a thioacetamide-induced hepatic fibrosis rat model.Magma (New York, N.Y.) · 2025Article
- Article
- From Pathophysiology to Practice: Evolving Pharmacological Therapies, Clinical Complications, and Pharmacogenetic Considerations in Portal Hypertension.Metabolites · 2025Review
- Effects of carvedilol on human prostate tissue contractility and stromal cell growth pointing to potential clinical implications.Pharmacological reports : PR · 2024Article
- Adrenoceptors and Hypertension.Handbook of experimental pharmacology · 2024Review
- Neuroimmunomodulation of adrenoblockers during liver cirrhosis: modulation of hepatic stellate cell activity.Annals of medicine · 2023Review
- Carvedilol impairs bile acid homeostasis in mice: implication for nonalcoholic steatohepatitis.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- Exploring the Potential Chemoprophylactic Role of Carvedilol for Hepatocellular Carcinoma.Gastroenterology & hepatology · 2022Article
- Protective Effect of Curcumin against Doxazosin- and Carvedilol-Induced Oxidative Stress in HepG2 Cells.Oxidative medicine and cellular longevity · 2022Article
- Doxazosin Attenuates Liver Fibrosis by Inhibiting Autophagy in Hepatic Stellate Cells via Activation of the PI3K/Akt/mTOR Signaling Pathway.Drug design, development and therapy · 2021Article
- Study on correlation between coagulation indexes and disease progression in patients with cirrhosis.American journal of translational research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Portal hypertension (PHT) is one of the most severe consequences of liver cirrhosis. Carvedilol is a first‑line pharmacological treatment of PHT. However, the antifibrogenic effects of carvedilol on liver cirrhosis and the intrinsic mechanisms underlying these effects have not been thoroughly investigated. The present study aimed to investigate the antifibrogenic effects of carvedilol on liver cirrhosis in vivo and in vitro. Liver cirrhosis was induced in rats by carbon tetrachloride (CCl4) administration for 9 weeks; carvedilol was administered simultaneously in the experimental group. Blood samples were collected for serum biochemistry. Liver tissues were used for fibrosis evaluation, histological examination, immunohistochemistry and western blot analysis. The human hepatic stellate cell (HSC) line LX‑2 was used for in vitro studies. The effects of carvedilol on LX‑2 cell proliferation and invasion were evaluated by Cell Counting Kit‑8 assay and Transwell invasion assays, respectively. The effect of carvedilol on transforming growth factor β1 (TGFβ1)‑induced collagen synthesis in LX‑2 cells and the molecular mechanisms were examined by western blot analysis. The results demonstrated that carvedilol improved CCl4‑induced structural distortion and fibrosis in the liver. Carvedilol inhibited HSC activation, proliferation and invasion. Carvedilol inhibited HSC collagen synthesis through the TGFβ1/SMAD pathway. In conclusion, carvedilol may alleviate liver cirrhosis in rats by inhibiting HSC activation, proliferation, invasion and collagen synthesis. Carvedilol may be a potential treatment of early‑stage liver cirrhosis.
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