ArticleThe American journal of pathology2000
Cytokeratin 8 protects from hepatotoxicity, and its ratio to cytokeratin 18 determines the ability of hepatocytes to form Mallory bodies.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 142 citations in OpenAlex.
- Role of SQSTM1/p62 in regulating Mallory-Denk body in alcohol-associated liver disease.eGastroenterology · 2025Article
- YTHDF2 facilitates aggresome formation via UPF1 in an mNature communications · 2023Article
- Association of Keratin 8 Level in Aqueous Humor With Outcomes of Intravitreal Ranibizumab Treatment for Neovascular Age-Related Macular Degeneration.Translational vision science & technology · 2022Article
- Priming, Triggering, Adaptation and Senescence (PTAS): A Hypothesis for a Common Damage Mechanism of Steatohepatitis.International journal of molecular sciences · 2021Article
- Different Roles of p62 (SQSTM1) Isoforms in Keratin-Related Protein Aggregation.International journal of molecular sciences · 2021Article
- The role of keratins in the digestive system: lessons from transgenic mouse models.Histochemistry and cell biology · 2018Review
- Alcohol induced hepatic degeneration in a hepatitis C virus core protein transgenic mouse model.International journal of molecular sciences · 2014Article
- Article
- Keratin 8 and 18 loss in epithelial cancer cells increases collective cell migration and cisplatin sensitivity through claudin1 up-regulation.The Journal of biological chemistry · 2013Article
- Keratin 8 phosphorylation regulates its transamidation and hepatocyte Mallory-Denk body formation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Costaining for keratins 8/18 plus ubiquitin improves detection of hepatocyte injury in nonalcoholic fatty liver disease.Human pathology · 2012Article
- Differentiation and selection of hepatocyte precursors in suspension spheroid culture of transgenic murine embryonic stem cells.PloS one · 2012Article
- The role of intracellular protein O-glycosylation in cell adhesion and disease.Journal of biomedical research · 2011Article
- Absence of keratin 8 confers a paradoxical microflora-dependent resistance to apoptosis in the colon.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Review
- Autophagy is involved in the elimination of intracellular inclusions, Mallory-Denk bodies, in hepatocytes.Medical molecular morphology · 2010Article
- Keratins modulate the shape and function of hepatocyte mitochondria: a mechanism for protection from apoptosis.Journal of cell science · 2009Article
- A cell culture system for the induction of Mallory bodies: Mallory bodies and aggresomes represent different types of inclusion bodies.Histochemistry and cell biology · 2009Article
- The human keratins: biology and pathology.Histochemistry and cell biology · 2008Review
- Intermediate filament cytoskeleton of the liver in health and disease.Histochemistry and cell biology · 2008Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In alcoholic hepatitis, a severe form of alcohol-induced toxic liver injury, as well as in experimental intoxication of mice with the porphyrinogenic drugs griseofulvin and 3,5-diethoxycarbonyl-1, 4-dihydrocollidine, hepatocytes form cytoplasmic protein aggregates (Mallory bodies; MBs) containing cytokeratins (CKs) and non-CK components. Here we report that mice lacking the CK8 gene and hence CK intermediate filaments in hepatocytes, but still expressing the type I partner, ie, the CK18 gene, do not form MBs but suffer from extensive porphyria and progressive toxic liver damage, leading to the death of a considerable number of animals (7 of 12 during 12 weeks of intoxication). Our observations show that 1) in the absence of CK8 as well as in the situation of a relative excess of CK18 over CK8 no MBs are formed; 2) the loss of CK8 is not compensated by other type II CKs; and 3) porphyria and toxic liver damage are drastically enhanced in the absence of CK8. Our results point to a protective role of CKs in certain types of toxic liver injury and suggest that MBs by themselves are not harmful to hepatocytes but may be considered as a product of a novel defense mechanism in hepatocytes.
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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.