ReviewNagoya journal of medical science2020
Chronic inflammation as a molecular basis of nonalcoholic steatohepatitis: role of macrophages and fibroblasts in the liver.
Review in Nagoya journal of medical science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed, 5 citations in OpenAlex.
- Silymarin and Inflammation: Food for Thoughts.Antioxidants (Basel, Switzerland) · 2024Review
- Improvement in insulin sensitivity and prevention of high fat diet-induced liver pathology using a CXCR2 antagonist.Cardiovascular diabetology · 2022Article
- PPARγ attenuates hepatic inflammation and oxidative stress of non‑alcoholic steatohepatitis via modulating the miR‑21‑5p/SFRP5 pathway.Molecular medicine reports · 2021Article
- Mitochondrial Lipid Homeostasis at the Crossroads of Liver and Heart Diseases.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathological spectrum of nonalcoholic fatty liver disease includes simple steatosis and nonalcoholic steatohepatitis (NASH), the latter of which is the leading cause of cirrhosis and hepatocellular carcinoma. The available evidence shows that parenchymal cell injury and death trigger inflammation and tissue fibrosis. During the development of liver fibrosis, stromal cells dramatically changes in their cellular component and activation status responding to hepatocyte injury due to various etiologies. It is important to understand how cell death induces chronic inflammation and fibrosis, and the disease-specific macrophages and fibroblasts responsible for NASH development under metabolic stress. This review discusses recent progress in the understanding the pathogenesis of NASH, focusing on disease-specific macrophages and fibroblasts.
Indexed as
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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.