SynthesisAlcohol, clinical & experimental research2025
Neutrophil extracellular traps (NETs) and NETosis in alcohol-associated diseases: A systematic review.
Synthesis in Alcohol, clinical & experimental research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- Gut-liver axis molecular mechanisms in alcohol-associated liver disease.Alcohol (Fayetteville, N.Y.) · 2026Review
- The versatile interplay between steatotic liver disease and liver cancer.Nature reviews. Cancer · 2026Review
- Interferon Regulatory Factors in Alcohol-Associated Liver Disease: Cell-Type Programs, Danger Signaling, and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Heavy alcohol consumption is implicated in the alteration of the antimicrobial function of neutrophils, such as phagocytosis, chemotaxis, the formation of neutrophil extracellular traps (NETs), and the occurrence of NETosis. NETosis is an endogenous process of elimination of invading microbes, autoantibodies, and inflammatory elements such as danger-associated molecular patterns (DAMPs) and pathogen-associated patterns (PAMPs). However, both exaggeration and suppression of NETosis modulate normal physiological and metabolic processes by influencing events at the molecular and cellular levels. Recent research shows that binge alcohol consumption induces NETosis, leading to tissue damage and inflammation. Binge alcohol consumption, chronic alcohol intake, and alcohol use disorder (AUD) can affect immunity and often lead to alcohol-associated liver disease (ALD) and/or other organ damage. Alcohol can lead to detrimental consequences in multiple organs, including the brain, liver, pancreas, and gut. Gut-derived microbial substances, such as endotoxins in the circulation, induce systemic inflammation. Sterile danger signals from damaged cells, cytokines, and prostaglandins act as proinflammatory stimuli and are involved in multiple signaling pathways. The alcohol-induced proinflammatory cytokines chemoattract neutrophils, which interact and coordinate with other immune cells to exaggerate or suppress inflammation within the inflammatory milieu, depending on the alcohol effects. Several proteins, including different receptors, play important roles in the activation and formation of NETs as well as the initiation and execution of NETosis. This review article specifically gathers the current information on NETosis, its biological components, and signaling pathways relating to the formation of NETs and the occurrence of NETosis associated with ALD and AUD in multiorgans, specifically in the brain, liver, and gut. We also briefly describe various therapeutic strategies against AUD-associated NETosis in experimental models and human disease states.
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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.