ReviewOncotarget2016
Tyrosine kinase inhibitors: friends or foe in treatment of hepatic fibrosis?
Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 14 citations in OpenAlex.
- Emerging Role of Ferroptosis in Chemotherapy-Associated Hepatorenal Toxicity: Mechanistic Insights and Toxicological Perspectives.ACS pharmacology & translational science · 2026Review
- Unveiling the Immunopharmacological Mechanisms of Biejiajian Pills (BJJP) Underlying the Treatment of Hepatic Fibrosis: Insights From Network Pharmacology and Experimental Validation.Food science & nutrition · 2026Article
- Drug Targeting and Nanomedicine: Lessons Learned from Liver Targeting and Opportunities for Drug Innovation.Pharmaceutics · 2022Review
- Lenvatinib prevents liver fibrosis by inhibiting hepatic stellate cell activation and sinusoidal capillarization in experimental liver fibrosis.Journal of cellular and molecular medicine · 2021Article
- Lyn kinase enhanced hepatic fibrosis by modulating the activation of hepatic stellate cells.American journal of translational research · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activity of tyrosine kinases has been proved to be associated with multiple diseases including fibrotic diseases. Tyrosine kinases inhibitors (TKIs) might be a novel approach to transform the anti-fibrotic treatment. However, both beneficial and adverse effects are observed by researchers when using these TKIs in either preclinical animal models or patients with hepatic fibrosis. Since hepatotoxicity of TKIs is the leading cause for drug withdrawals thus limits its application in anti-fibrosis, not only efficacy but also safety of TKIs should be paid great concerns. It has been observed in a few studies that TKIs could induce relatively high rate of hepatic biochemical markers elevations and even result in liver failure. Fortunately, several strategies have been adopt to handle with the hepatotoxicity. Accumulating evidences suggest that hepatic stellate cells (HSC) play a pivotal role in hepatic fibrogenesis, so it might be a good option to develop selective TKIs specifically targeting HSCs. The present review will briefly summarize the anti-fibrotic mechanism of TKIs, adverse effects of TKIs as well as the novel developed selective delivery of TKIs.
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What OpenQuestion holds
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.