ArticleCell death & disease2019
Hepatic ferroptosis plays an important role as the trigger for initiating inflammation in nonalcoholic steatohepatitis.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 papers, 1 of them a synthesis that pooled it.
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Who cites it
297 citing papers in PubMed, 1 synthesis or guideline pooled it, 492 citations in OpenAlex.
- Bibliometric analysis and visualization of ferroptosis in metabolic dysfunction-associated steatotic liver disease (MASLD): a comprehensive review.Frontiers in pharmacology · 2026Pooled it
- Exploring Ferroptosis: A Key Mechanism in Respiratory System Diseases and its Therapeutic Potential.Applied biochemistry and biotechnology · 2026Review
- Ferroptosis in liver biology and diseases.Hepatology communications · 2026Review
- Cordycepin Alleviates Non Alcoholic Fatty Liver Disease Progression by Stabilizing GCH1 to Inhibit Ferroptosis.Phytotherapy research : PTR · 2026Article
- Ferroptosis and Ferro-Aging in Obesity: Bibliometric Mapping, Shared Mechanisms, and Translational Perspectives.Metabolites · 2026Review
- Potential Therapeutic Roles of Icariin in Inflammatory Diseases: From Molecular Mechanisms to Clinical Translation Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- Sinomenine protects mice againstMicrobiology spectrum · 2026Article
- Molecular mechanisms of iron metabolism and ferroptosis in cardiovascular diseases and intervention strategies targeting natural products (Review).Molecular medicine reports · 2026Review
- Molecular Pathophysiology of Hepatocellular Carcinoma: From Metabolic Inflammation to Therapeutic Targets.Cancers · 2026Review
- Macrophage Notch1 drives hepatocyte ferroptosis via the exosomal miR-142a-3p/TIPE2 axis to promote MASH progression.Cell & bioscience · 2026Article
- Context-Dependent Modulation of Ferroptosis by Metformin: Mechanisms, Therapeutic Implications and Open Questions.Pharmaceuticals (Basel, Switzerland) · 2026Review
- L-2-Hydroxyglutarate sensitizes ferroptosis through ATF3/CHAC1-mediated glutathione degradation in hepatocellular carcinoma.Cell death & disease · 2026Article
- Exercise-Induced Hepatic Mitochondrial Reprogramming Across Muscle-Gut-Thyroid Axes in MASLD/MASH.International journal of molecular sciences · 2026Review
- Mapping lipid droplet viscosity: A novel tool for spatiotemporal ferroptosis imaging: Editorial on "Novel near-infrared probe for monitoring lipid peroxidation-mediated viscosity change in ferroptotic hepatocytes".Clinical and molecular hepatology · 2026Article
- ACSL4 in Alzheimer's disease: Pathogenetic mechanisms and potential therapeutic targets.Genes & diseases · 2026Review
- Identification of circadian rhythm-associated key genes in metabolic dysfunction-associated fatty liver disease.Clinical and experimental medicine · 2026Article
- Preconditioning with sufentanil confers protective effects in transplantation by attenuating hepatic ischemia-reperfusion injury.World journal of transplantation · 2026Review
- Tacrolimus Inhibits Hepatic Ferroptosis Through Modulating SIRT7-Dependent NRF2 Activation in Diabetes.Antioxidants (Basel, Switzerland) · 2026Article
- Pirfenidone Sensitizes Hepatic Stellate Cells to Ferroptosis by Reprogramming Glutamine and Serine Metabolism for GSH Depletion.Antioxidants (Basel, Switzerland) · 2026Article
- Redox Imbalance in the Cardiohepatic Syndrome: The Emerging Role of Oxidative Stress in Cirrhosis-Associated Cardiac Dysfunction.Antioxidants (Basel, Switzerland) · 2026Review
237 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic steatohepatitis (NASH) is a metabolic liver disease that progresses from simple steatosis to the disease state of inflammation and fibrosis. Previous studies suggest that apoptosis and necroptosis may contribute to the pathogenesis of NASH, based on several murine models. However, the mechanisms underlying the transition of simple steatosis to steatohepatitis remain unclear, because it is difficult to identify when and where such cell deaths begin to occur in the pathophysiological process of NASH. In the present study, our aim is to investigate which type of cell death plays a role as the trigger for initiating inflammation in fatty liver. By establishing a simple method of discriminating between apoptosis and necrosis in the liver, we found that necrosis occurred prior to apoptosis at the onset of steatohepatitis in the choline-deficient, ethionine-supplemented (CDE) diet model. To further investigate what type of necrosis is involved in the initial necrotic cell death, we examined the effect of necroptosis and ferroptosis inhibition by administering inhibitors to wild-type mice in the CDE diet model. In addition, necroptosis was evaluated using mixed lineage kinase domain-like protein (MLKL) knockout mice, which is lacking in a terminal executor of necroptosis. Consequently, necroptosis inhibition failed to block the onset of necrotic cell death, while ferroptosis inhibition protected hepatocytes from necrotic death almost completely, and suppressed the subsequent infiltration of immune cells and inflammatory reaction. Furthermore, the amount of oxidized phosphatidylethanolamine, which is involved in ferroptosis pathway, was increased in the liver sample of the CDE diet-fed mice. These findings suggest that hepatic ferroptosis plays an important role as the trigger for initiating inflammation in steatohepatitis and may be a therapeutic target for preventing the onset of steatohepatitis.
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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.