ArticleThe Journal of biological chemistry2014
Age-associated change of C/EBP family proteins causes severe liver injury and acceleration of liver proliferation after CCl4 treatments.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Identification of biomarkers associated with coronary artery disease and non-alcoholic fatty liver disease by bioinformatics analysis and machine learning.Scientific reports · 2025Article
- Genetic Ablation of C/EBPα-p300 Pathway Blocks Development of Obese Pregnancy Associated Liver Disorders in Offspring.Cellular and molecular gastroenterology and hepatology · 2024Article
- Magnesium and Liver Metabolism Through the Lifespan.Advances in nutrition (Bethesda, Md.) · 2023Review
- Administration of Glutaredoxin-1 Attenuates Liver Fibrosis Caused by Aging and Non-Alcoholic Steatohepatitis.Antioxidants (Basel, Switzerland) · 2022Article
- CCAAT/Enhancer-Binding Proteins in Fibrosis: Complex Roles Beyond Conventional Understanding.Research (Washington, D.C.) · 2022Review
- The Dynamic Interplay Between Mast Cells, Aging/Cellular Senescence, and Liver Disease.Gene expression · 2020Review
- Aging Suppresses Sphingosine-1-Phosphate Chaperone ApoM in Circulation Resulting in Maladaptive Organ Repair.Developmental cell · 2020Article
- Hepatoprotective Effects of Standardized Extracts from an Ancient Italian Apple Variety (Mela Rosa dei Monti Sibillini) against Carbon Tetrachloride (CClMolecules (Basel, Switzerland) · 2020Article
- Weaning Mice and Adult Mice Exhibit Differential Carbon Tetrachloride-Induced Acute Hepatotoxicity.Antioxidants (Basel, Switzerland) · 2020Article
- Protective Effects of Nutria Bile against Thioacetamide-Induced Liver Injury in Mice.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- Identifying and Implementing Endpoints for Geriatric Mice.Comparative medicine · 2018Article
- Role of lncRNAs in aging and age-related diseases.Aging medicine (Milton (N.S.W)) · 2018Review
- Gene activation of CEBPA using saRNA: preclinical studies of the first in human saRNA drug candidate for liver cancer.Oncogene · 2018Article
- Gankyrin Promotes Tumor-Suppressor Protein Degradation to Drive Hepatocyte Proliferation.Cellular and molecular gastroenterology and hepatology · 2018Article
- The Role of Saikosaponins in Therapeutic Strategies for Age-Related Diseases.Oxidative medicine and cellular longevity · 2018Review
- RNA Binding Protein CUGBP1 Inhibits Liver Cancer in a Phosphorylation-Dependent Manner.Molecular and cellular biology · 2017Article
- Aging of the Liver: What This Means for Patients with HIV.Current HIV/AIDS reports · 2016Review
- CUG-binding protein 1 regulates HSC activation and liver fibrogenesis.Nature communications · 2016Article
- p300 Regulates Liver Functions by Controlling p53 and C/EBP Family Proteins through Multiple Signaling Pathways.Molecular and cellular biology · 2015Article
- Aging and liver disease.Current opinion in gastroenterology · 2015Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The aged liver is more sensitive to the drug treatments and has a high probability of developing liver disorders such as fibrosis, cirrhosis, and cancer. Here we present mechanisms underlying age-associated severe liver injury and acceleration of liver proliferation after CCl4 treatments. We have examined liver response to CCl4 treatments using old WT mice and young C/EBPα-S193D knockin mice, which express an aged-like isoform of C/EBPα. Both animal models have altered chromatin structure as well as increased liver injury and proliferation after acute CCl4 treatments. We found that these age-related changes are associated with the repression of key regulators of liver biology: C/EBPα, Farnesoid X Receptor (FXR) and telomere reverse transcriptase (TERT). In quiescent livers of old WT and young S193D mice, the inhibition of TERT is mediated by HDAC1-C/EBPα complexes. After CCl4 treatments, TERT, C/EBPα and FXR are repressed by different mechanisms. These mechanisms include the increase of a dominant negative isoform, C/EBPβ-LIP, and subsequent repression of C/EBPα, FXR, and TERT promoters. C/EBPβ-LIP also disrupts Rb-E2F1 complexes in C/EBPα-S193D mice after CCl4 treatments. To examine if these alterations are involved in drug-mediated liver diseases, we performed chronic treatments of mice with CCl4. We found that C/EBPα-S193D mice developed fibrosis much more rapidly than WT mice. Thus, our data show that the age-associated alterations of C/EBP proteins create favorable conditions for the increased liver proliferation after CCl4 treatments and for development of drug-mediated liver diseases.
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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.