ArticleTherapeutic advances in gastroenterology2011
Current status of novel antifibrotic therapies in patients with chronic liver disease.
Article in Therapeutic advances in gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
What it found
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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
78 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Use of anti-platelet agents in the prevention of hepatic fibrosis in patients at risk for chronic liver disease: a systematic review and meta-analysis.Hepatology international · 2019Pooled it
- Advances in the study of the mechanism of action of miR‑22 in liver lesions (Review).Oncology letters · 2024Review
- Therapeutic potential of oleanolic acid in liver diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Inhibitory Effects ofAntioxidants (Basel, Switzerland) · 2023Article
- Cell-Permeable PROTAC Degraders against KEAP1 Efficiently Suppress Hepatic Stellate Cell Activation through the Antioxidant and Anti-Inflammatory Pathway.ACS pharmacology & translational science · 2023Article
- The effects of N-acetylcysteine on hepatic, hematologic, and renal parameters in cirrhotic patients: a randomized controlled trial.Gastroenterology and hepatology from bed to bench · 2023Article
- Role and mechanism of DNA methylation and its inhibitors in hepatic fibrosis.Frontiers in genetics · 2023Review
- RETRACTED: Adenine Combined with Cisplatin Promotes Anticancer Activity against Hepatocellular Cancer Cells through AMPK-Mediated p53/p21 and p38 MAPK Cascades.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Article
- Myocardin and myocardin-related transcription factor-A synergistically mediate actin cytoskeletal-dependent inhibition of liver fibrogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2020Article
- Antioxidant, anti-inflammatory and anti-fibrotic effects ofExperimental and therapeutic medicine · 2020Article
- Article
- Tissue transglutaminase 2 regulates tumor cell tensional homeostasis by increasing contractility.Journal of cell science · 2020Article
- Exploring the Role ofFrontiers in bioengineering and biotechnology · 2020Article
- Article
- Targeted Delivery of an siRNA/PNA Hybrid Nanocomplex Reverses Carbon Tetrachloride-Induced Liver Fibrosis.Advanced therapeutics · 2019Article
- The circadian clock and liver function in health and disease.Journal of hepatology · 2019Review
- B-mode ultrasound for the assessment of hepatic fibrosis: a quantitative multiparametric analysis for a radiomics approach.Scientific reports · 2019Article
- Umbelliferone Ameliorates CClInflammation · 2019Article
- Swertiamarin ameliorates carbon tetrachloride-induced hepatic apoptosisThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis accumulation is a dynamic process resulting from a wound-healing response to acute or chronic liver injury of all causes. The cascade starts with hepatocyte necrosis and apoptosis, which instigate inflammatory signaling by chemokines and cytokines, recruitment of immune cell populations, and activation of fibrogenic cells, culminating in the deposition of extracellular matrix. These key elements, along with pathways of transcriptional and epigenetic regulation, represent fertile therapeutic targets. New therapies include drugs specifically designed as antifibrotics, as well as drugs already available with well-established safety profiles, whose mechanism of action may also be antifibrotic. At the same time, the development of noninvasive fibrogenic markers, and techniques (e.g. fibroscan), as well as combined scoring systems incorporating serum and clinical features will allow improved assessment of therapy response. In aggregate, the advances in the elucidation of the biology of fibrosis, combined with improved technologies for assessment will provide a comprehensive framework for design of antifibrotics and their analysis in well-designed clinical trials. These efforts may ultimately yield success in halting the progression of, or reversing, 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.