ReviewDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2026
Hepatic stellate cells in alcoholic liver cirrhosis: mechanisms of fibrogenesis, plasticity, and fibrosis reversal.
Review in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTo critically synthesize current mechanistic and clinical evidence on the role of hepatic stellate cells (HSCs) in alcoholic liver cirrhosis, with emphasis on fibrogenesis, cellular plasticity, fibrosis regression, and emerging diagnostic implications. EVIDENCE ACQUISITION: A narrative review of literature was conducted using PubMed, Scopus, and Web of Science to identify relevant studies on hepatic stellate cells and their role in liver cirrhosis, with emphasis on recent mechanistic and translational research.
resultsHSCs are central mediators of fibrogenesis in alcoholic liver disease, contributing to extracellular matrix remodeling, immune signaling, and vascular alterations. Emerging evidence highlights the dynamic and potentially reversible nature of HSC activation, with distinct roles for apoptosis, senescence, and inactivation pathways. Recent studies also emphasize the influence of metabolic stress, gut-liver axis interactions, and micronutrient imbalances on HSC behavior. These insights support the development of targeted antifibrotic strategies and biomarker-driven approaches for disease monitoring.
conclusionHSCs are central drivers of fibrogenesis, vascular remodeling, and immune metabolic crosstalk in alcoholic liver cirrhosis. Integrating HSC-focused molecular profiling with non-invasive diagnostics and robust clinical endpoints is essential for the development of effective antifibrotic strategies.
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