ReviewCellular and molecular gastroenterology and hepatology2015
Alcoholic, Nonalcoholic, and Toxicant-Associated Steatohepatitis: Mechanistic Similarities and Differences.
Review in Cellular and molecular gastroenterology and hepatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed.
- Review
- Article
- 35k Da specific-sized hyaluronan ameliorates high-fat diet-induced liver injury in murine model of moderate obesity.Matrix biology : journal of the International Society for Matrix Biology · 2025Article
- Quantitative proteomic analysis unveils a critical role of VARS1 in hepatocellular carcinoma aggressiveness through the modulation of MAGI1 expression.Molecular cancer · 2025Article
- Inflammatory and metabolic markers mediate the association between urinary metals and non-alcoholic fatty liver disease in U.S. adults: a cross-sectional study.Frontiers in public health · 2025Article
- Review
- Dietary therapy of murine primary biliary cholangitis induces hepatocellular steatosis: A cautionary tale.Liver international : official journal of the International Association for the Study of the Liver · 2024Article
- Immunological mechanisms in steatotic liver diseases: An overview and clinical perspectives.Clinical and molecular hepatology · 2024Review
- Alcohol-Associated Liver Disease Outcomes: Critical Mechanisms of Liver Injury Progression.Biomolecules · 2024Review
- Obesogenic polystyrene microplastic exposures disrupt the gut-liver-adipose axis.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Role of intestinal flora in the development of nonalcoholic fatty liver disease in children.Microbiology spectrum · 2024Article
- Contributing roles of mitochondrial dysfunction and hepatocyte apoptosis in liver diseases through oxidative stress, post-translational modifications, inflammation, and intestinal barrier dysfunction.Cellular and molecular life sciences : CMLS · 2024Review
- Alcohol-associated liver disease and behavioral and medical cofactors: unmet needs and opportunities.Frontiers in public health · 2024Review
- Intestinal Barrier Function in the Pathogenesis of Nonalcoholic Fatty Liver Disease.Journal of clinical and translational hepatology · 2023Review
- Transcriptomic analysis in zebrafish larvae identifies iron-dependent mitochondrial dysfunction as a possible key event of NAFLD progression induced by benzo[a]pyrene/ethanol co-exposure.Cell biology and toxicology · 2023Article
- A New In Vivo Zebrafish Bioassay Evaluating Liver Steatosis Identifies DDE as a Steatogenic Endocrine Disruptor, Partly through SCD1 Regulation.International journal of molecular sciences · 2023Article
- Alcohol-Related Liver Disease: An Overview on Pathophysiology, Diagnosis and Therapeutic Perspectives.Biomedicines · 2022Review
- Environmental Toxicants and NAFLD: A Neglected yet Significant Relationship.Digestive diseases and sciences · 2022Review
- Xenobiotic-Induced Aggravation of Metabolic-Associated Fatty Liver Disease.International journal of molecular sciences · 2022Review
- Immunometabolic factors contributing to obesity-linked hepatocellular carcinoma.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Hepatic steatosis and steatohepatitis are common histologic findings that can be caused by multiple etiologies. The three most frequent causes for steatosis/steatohepatitis are alcohol (alcoholic steatohepatitis, ASH), obesity/metabolic syndrome (nonalcoholic steatohepatitis, NASH), and environmental toxicants (toxicant-associated steatohepatitis, TASH). Hepatic steatosis is an early occurrence in all three forms of liver disease, and they often share common pathways to disease progression/severity. Disease progression is a result of both direct effects on the liver as well as indirect alterations in other organs/tissues such as intestine, adipose tissue, and the immune system. Although the three liver diseases (ASH, NASH, and TASH) share many common pathogenic mechanisms, they also exhibit distinct differences. Both shared and divergent mechanisms can be potential therapeutic targets. This review provides an overview of selected important mechanistic similarities and differences in ASH, NASH, and TASH.
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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.