ReviewClinics and research in hepatology and gastroenterology2015
New therapies for hepatic fibrosis.
Review in Clinics and research in hepatology and gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
- Tolerability and Pharmacokinetics of Hydronidone, an Antifibrotic Agent for Hepatic Fibrosis, after Single and Multiple Doses in Healthy Subjects: an Open-Label, Randomized, Dose-Escalating, First-in-Human Study.European journal of drug metabolism and pharmacokinetics · 2017Trial
- Preparation of Oral Artesunate-Chitosan Oligosaccharide-Retinoic Acid Copolymer Micelles for Attenuating Hepatic Fibrosis.Pharmaceutics · 2026Article
- Co-Assembled Nanoparticles Comprising Sorafenib and Hederagenin Derivative for Enhanced Anti-Hepatic Fibrosis Activity.International journal of nanomedicine · 2025Article
- Exosome-mediated delivery of Cas9 ribonucleoprotein complexes for tissue-specific gene therapy of liver diseases.Science advances · 2022Article
- Established Liposome-Coated IMB16-4 Polymeric Nanoparticles (LNPs) for Increasing Cellular Uptake and Anti-Fibrotic Effects In Vitro.Molecules (Basel, Switzerland) · 2022Article
- XSSJS inhibits hepatic fibrosis by promoting the miR-29b-3p/VEGFA axis in vitro and in vivo.Bioscience reports · 2022Article
- Peroxidasin Deficiency Re-programs Macrophages Toward Pro-fibrolysis Function and Promotes Collagen Resolution in Liver.Cellular and molecular gastroenterology and hepatology · 2022Article
- Development of a novel anti-liver fibrosis formula with luteolin, licochalcone A, aloe-emodin and acacetin by network pharmacology and transcriptomics analysis.Pharmaceutical biology · 2021Article
- Alisma Shugan Decoction (ASD) Ameliorates Hepatotoxicity and Associated Liver Dysfunction by Inhibiting Oxidative Stress and p65/Nrf2/JunD Signaling Dysregulation In Vivo.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- A Lipidomic Analysis of Docosahexaenoic Acid (22:6, ω3) Mediated Attenuation of Western Diet Induced Nonalcoholic Steatohepatitis in MaleMetabolites · 2019Article
- Alpha Mangostin Inhibits the Proliferation and Activation of Acetaldehyde Induced Hepatic Stellate Cells through TGF-Journal of toxicology · 2018Article
- Omega-3 polyunsaturated fatty acids as a treatment strategy for nonalcoholic fatty liver disease.Pharmacology & therapeutics · 2018Review
- Microarray analysis of differentially expressed genes in L929 mouse fibroblast cells exposed to leptin and hypoxia.Molecular medicine reports · 2017Article
- MicroRNA-29a Alleviates Bile Duct Ligation Exacerbation of Hepatic Fibrosis in Mice through Epigenetic Control of Methyltransferases.International journal of molecular sciences · 2017Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Liver fibrosis is an outcome of many chronic diseases, and often results in cirrhosis, liver failure, and portal hypertension. Liver transplantation is the only treatment available for patients with advanced stages of liver cirrhosis. Therefore, alternative methods are required to develop new strategies for anti-fibrotic therapy. Various kinds of hepatocyte injuries cause inflammatory reactions, which lead to activation of hepatic stellate cells (HSCs). Continuous liver injuries maintain these activated HSCs, and they are called as myofibroblasts. Myofibroblasts proliferate in response to various kinds of cytokines and produce extracellular matrix proteins (ECMs). Myofibroblasts undergo apoptosis and inactivation when the underlying causative etiologies are cleared. Here, we describe the current knowledge of targeting the activated HSCs as a therapeutic target for liver fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.