ReviewPhysiological reviews2010
Hepatocyte death: a clear and present danger.
Review in Physiological reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 211 papers.
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
211 citing papers in PubMed, 468 citations in OpenAlex.
- Redox Reprogramming of the Diseased Liver by Dietary Flavonoids: From Molecular Signalling to Gut-Liver Crosstalk.Biology · 2026Review
- Long-term supplementation of exogenous bile acids enhanced growth efficacy, hematology, non-specific immunity, and intestinal histomorphology, with significant liver dysfunction in Nile tilapia fingerlings.Veterinary research communications · 2026Article
- Self-assembled PEGylated nanoparticles based on Elafibranor derivative 3d for the treatment of metabolic dysfunction-associated steatohepatitis.Journal of biological engineering · 2026Article
- Network pharmacology, molecular docking, molecular dynamics simulation, and in vivo experiments elucidate the potential mechanisms of berberine against liver injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- piR-16404 drives ferroptotic liver injury via CASTOR1/mTORC1/GPX4 dysregulation in HepG2 cells and mice: a novel toxicity mechanism of N, N-dimethylformamide.Archives of toxicology · 2026Article
- Hepatocyte-Derived Apoptotic Bodies as Pathological Intercellular Messengers in the Liver.Biomolecules · 2026Review
- Shifting cell death modes in hepatic steatosis: from apoptosis to necroptosis.Endocrine journal · 2026Review
- Modulation of Oxidative and ER Stress Pathways by the ADAM17 Inhibitor GW280264X in LPS-Induced Acute Liver Injury.Life (Basel, Switzerland) · 2025Article
- Ferroptosis in liver fibrosis and its potential intervention strategy.Cell biology and toxicology · 2025Review
- Elucidating the Mechanism of Liver and Kidney Damage in Rats Caused by Exposure to 2,4-Dichlorophenoxyacetic Acid and the Protective Effect ofInternational journal of molecular sciences · 2025Article
- Vitamin A toxicity and hepatic pathology: A comprehensive review.World journal of hepatology · 2025Review
- SARS-CoV-2 Main Protease Dysregulates Hepatic Insulin Signaling and Glucose Uptake: Implications for Post-COVID-19 Diabetogenesis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Article
- Inhibition RIP1 prevents acute liver failure by suppressing hepatic apoptosis and attenuating the secretion of TNF-α from macrophages.European journal of medical research · 2025Article
- Targeting Lipophagy in Liver Diseases: Impact on Oxidative Stress and Steatohepatitis.Antioxidants (Basel, Switzerland) · 2025Review
- High Temperature and Ethinylestradiol May Reduce Body Growth, Liver and Hepatocyte Volumes and Lipid Droplets in Adult Male Guppies.Animals : an open access journal from MDPI · 2025Article
- MtDNA 3243 A>G mutation and recurrent cholangitis after Kasai procedure in biliary atresia: a case report.Translational pediatrics · 2025Article
- Suppression of stress granule formation is a vulnerability imposed by mutant p53.Nature communications · 2025Article
- Sinusoidal communication in chronic liver disease.Clinical and molecular hepatology · 2025Review
- Sweroside: unveiling broad therapeutic potential-from mechanistic insights to clinical potential.Frontiers in pharmacology · 2025Review
- A p21-ATD mouse model for monitoring and eliminating senescent cells and its application in liver regeneration post injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
151 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
3 authors at 1 institution in 1 country.
Funding
Abstract
The hepatocyte is especially vulnerable to injury due to its central role in xenobiotic metabolism including drugs and alcohol, participation in lipid and fatty acid metabolism, its unique role in the enterohepatic circulation of bile acids, the widespread prevalence of hepatotropic viruses, and its existence within a milieu of innate immune responding cells. Apoptosis and necrosis are the most widely recognized forms of hepatocyte cell death. The hepatocyte displays many unique features regarding cell death by apoptosis. It is quite susceptible to death receptor-mediated injury, and its death receptor signaling pathways involve the mitochondrial pathway for efficient cell killing. Also, death receptors can trigger lysosomal disruption in hepatocytes which further promote cell and tissue injury. Interestingly, hepatocytes are protected from cell death by only two anti-apoptotic proteins, Bcl-x(L) and Mcl-1, which have nonredundant functions. Endoplasmic reticulum stress or the unfolded protein response contributes to hepatocyte cell death during alterations of lipid and fatty acid metabolism. Finally, the current information implicating RIP kinases in necrosis provides an approach to more fully address this mode of cell death in hepatocyte injury. All of these processes contributing to hepatocyte injury are discussed in the context of potential therapeutic strategies.
Indexed as
Identifiers
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.