ReviewFrontiers in pharmacology2022
Roles of hepatic stellate cells in NAFLD: From the perspective of inflammation and fibrosis.
Review in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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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
39 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Efficacy of Telmisartan in MASLD/NAFLD: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.Endocrinology, diabetes & metabolism · 2026Pooled it
- E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Inflammation burden index as a complementary marker for the assessment of hepatic steatosis and fibrosis: evidence from NHANES 2017-2018.Abdominal radiology (New York) · 2026Article
- Liver fibrosis risk: a silent threat in type 1 diabetes mellitus.Journal of endocrinological investigation · 2026Article
- Composite dietary antioxidant index and risk of metabolic dysfunction - associated steatotic liver disease: evidence from a prospective cohort study.Nutrition & metabolism · 2026Article
- hs-CRP as a Marker of Systemic Low-Grade Inflammation Is Not Associated with Steatotic Liver Disease in Adolescents: Insights from the EVA4YOU Study.Metabolites · 2026Article
- Orphan drug uttroside B impedes MASH progression and HCC development in experimental models.JHEP reports : innovation in hepatology · 2026Article
- The double-edged sword of regulatory T cells in MASLD: from inflammation control to fibrosis promotion.Animal cells and systems · 2026Review
- Newly identified single-nucleotide polymorphism associated with the transition from nonalcoholic fatty liver disease to liver fibrosis: results from a nested case-control study in the UK biobank.Annals of medicine · 2025Article
- The Adverse Impact of Pregestational Prediabetes Contributes to HELLP Syndrome Development.Biology · 2025Article
- Toxins to treatments: Impact of environmental pollutants, gut microbiota, and natural compounds on non-alcoholic fatty liver disease progression.World journal of hepatology · 2025Review
- Quantitative longitudinal investigation of non-alcoholic steatohepatitis in mice by photoacoustic microscopy.Photoacoustics · 2025Article
- Hepatic stellate cell inhibition by angiotensin II receptor blocker mitigates liver injury and fibrosis via NF-κB-galectin-3 suppression in a rat nonalcoholic steatohepatitis model.Archives of toxicology · 2025Article
- Liver and pancreatic fat fractions as predictors of disease severity in acute pancreatitis: an MRI IDEAL-IQ study.Abdominal radiology (New York) · 2025Article
- Hepatic stellate cell-specific Kcnma1 deletion mitigates metabolic dysfunction-associated steatotic liver disease progression via upregulating Amphiregulin secretion.Molecular metabolism · 2025Article
- Hesperidin Is a Promising Nutraceutical Compound in Counteracting the Progression of NAFLD In Vitro.International journal of molecular sciences · 2025Article
- Quercetagetin alleviates liver fibrosis in non-alcoholic fatty liver disease by promoting ferroptosis of hepatic stellate cells through GPX4 ubiquitination.Chinese medicine · 2025Article
- Endoplasmic reticulum stress sensor protein PERK in hepatic stellate cells promotes the progression of hepatocellular carcinoma via p38δ MAPK/IL-1β axis.Scientific reports · 2025Article
- Clinical characteristics of MASLD/MetALD/MAFLD/NAFLD and the relative risk analysis on metabolic disorders.BMC gastroenterology · 2025Article
- Association of advanced lung cancer inflammation index with all-cause and cardiovascular mortality in metabolic dysfunction associated steatotic liver disease.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic fatty liver disease (NAFLD) has become one of the most common diseases and severe problems worldwide because of the global increase in obesity, dyslipidemia, hypertension, and type 2 diabetes mellitus. NAFLD includes a wide spectrum of liver diseases, the histological forms of which range from non-alcoholic fatty liver (NAFL), which is generally nonprogressive, to non-alcoholic steatohepatitis (NASH), which can progress to chronic hepatitis, liver cirrhosis (LC), and sometimes hepatocellular carcinoma (HCC). Unlike NAFL, as the progressive form of NAFLD, NASH is characterized by the presence of inflammation with or without fibrosis in addition to hepatic steatosis. Although it is widely known and proved that persistent hepatic injury and chronic inflammation in the liver activate quiescent hepatic stellate cells (HSCs) and lead to hepatic fibrosis, the three-step process of "inflammation-fibrosis-carcinoma" in NAFLD has not been investigated and clarified clearly. In this process, the initiation of inflammation in the liver and the function of various liver inflammatory cells have been discussed regularly, while the activated HSCs, which constitute the principal cells responsible for fibrosis and their cross-talk with inflammation, seem not to be investigated specifically and frequently. Also, accumulated evidence suggests that HSCs can not only be activated by inflammation but also participate in the regulation of liver inflammation. Therefore, it is necessary to investigate the unique roles of HSCs in NAFLD from the perspective of inflammation and fibrosis. Here, we review the pivotal effects and mechanisms of HSCs and highlight the potential value of HSC-targeted treatment methods in NAFLD.
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