ReviewJournal of hepatology2019
Inflammatory pathways in alcoholic steatohepatitis.
Review in Journal of hepatology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers, 1 of them a synthesis that pooled it.
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
229 citing papers in PubMed, 1 synthesis or guideline pooled it, 366 citations in OpenAlex.
- Inflammatory cytokines and alcohol use disorder: systematic review and meta-analysis.Revista brasileira de psiquiatria (Sao Paulo, Brazil : 1999) · 2022Pooled it
- Trial
- Alcohol Consumption Is Associated with Poor Prognosis in Obese Patients with COVID-19: A Mendelian Randomization Study Using UK Biobank.Nutrients · 2021Trial
- The convergent roles of metabolic dysfunction, alcohol, and iron in steatotic liver disease: a review.Bioscience reports · 2026Review
- Timing and trajectory of acute kidney injury predict mortality in alcohol-associated hepatitis: A multinational cohort study.Hepatology communications · 2026Article
- Differential Associations of Dietary Inflammatory Index and Dietary Antioxidant Indices With Mortality Risk From MASLD/MetALD: Results From a Large Population-Based Study.Food science & nutrition · 2026Article
- Macrophage ACAT1 Aggravates Alcohol-Associated Liver Disease by Inducing Mitochondrial Damage and NLRP3 Activation.Journal of gastroenterology and hepatology · 2026Article
- Prognostic Utility of Systemic Inflammatory Response Syndrome (SIRS) Criteria in Acute Alcohol-Associated Hepatitis.Digestive diseases and sciences · 2026Article
- Platelet-derived S100A9 contributes to endotheliopathy in alcohol-associated hepatitis.JCI insight · 2026Article
- [Alcohol liver disease: immunoregulatory mechanisms and precision therapeutic targets].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Astaxanthin Vesicles Improve Alcoholic Liver Disease Through Oxidative Stress and NF-κB Inflammatory Pathway.Food science & nutrition · 2026Article
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
- The versatile interplay between steatotic liver disease and liver cancer.Nature reviews. Cancer · 2026Review
- Serum HMGB1 and Alcohol-Related Liver Disease.Journal of clinical medicine · 2026Article
- Genetic regulation of AIF1 shapes immune and liver injury profiles in chronic alcohol use.JCI insight · 2026Article
- Oxidative Stress and Alcohol-Related Hepatitis: A Role for Future Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Short-term time-restricted feeding improves metabolic rhythms and liver mitochondrial bioenergetic function in high-fat diet-fed mice.Function (Oxford, England) · 2026Article
- Emerging therapeutic regimens as alternatives to glucocorticoids for severe alcohol-associated hepatitis: a comprehensive review.Clinical and molecular hepatology · 2026Review
- Metabolic Reprogramming Driven by Modifiable Lifestyle Factors in Metabolic Syndrome and Alcohol-Related Liver Disease: A Narrative Review.Metabolites · 2026Review
- A preclinical candidate of cyclophilin D inhibition improves alcohol-associated liver injury.Cell reports. Medicine · 2026Article
169 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
4 authors at 4 institutions in 1 country.
Funding
Abstract
Inflammatory processes are primary contributors to the development and progression of alcoholic steatohepatitis (ASH), with severe alcoholic hepatitis characterised by non-resolving inflammation. Inflammation in the progression of ASH is a complex response to microbial dysbiosis, loss of barrier integrity in the intestine, hepatocellular stress and death, as well as inter-organ crosstalk. Herein, we review the roles of multiple cell types that are involved in inflammation in ASH, including resident macrophages and infiltrating monocytes, as well as other cell types in the innate and adaptive immune system. In response to chronic, heavy alcohol exposure, hepatocytes themselves also contribute to the inflammatory process; hepatocytes express a large number of chemokines and inflammatory mediators and can also release damage-associated molecular patterns during injury and death. These cellular responses are mediated and accompanied by changes in the expression of pro- and anti-inflammatory cytokines and chemokines, as well as by signals which orchestrate the recruitment of immune cells and activation of the inflammatory process. Additional mechanisms for cell-cell and inter-organ communication in ASH are also reviewed, including the roles of extracellular vesicles and microRNAs, as well as inter-organ crosstalk. We highlight the concept that inflammation also plays an important role in promoting liver repair and controlling bacterial infection. Understanding the complex regulatory processes that are disrupted during the progression of ASH will likely lead to better targeted strategies for therapeutic interventions.
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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.