ArticleExperimental biology and medicine (Maywood, N.J.)2012
Oxidative stress contributes to liver damage in a murine model of alpha-1-antitrypsin deficiency.
Article in Experimental biology and medicine (Maywood, N.J.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Understanding the role of hypoxia inducible factors in liver fibrosis and future therapeutic applications.iLIVER · 2026Review
- RNA editing for the treatment of alpha-1 antitrypsin deficiency.Nucleic acids research · 2026Article
- Pioglitazone reduces hepatic α-1 antitrypsin accumulation through autophagy and AMPK activation in α-1 antitrypsin-deficient mice.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Sirtuin3 promotes the degradation of hepatic Z alpha-1 antitrypsin through lipophagy.Hepatology communications · 2024Article
- Oxidative Stress in Liver Pathophysiology and Disease.Antioxidants (Basel, Switzerland) · 2023Review
- The Role of Oxidative Stress and Antioxidants in Cardiovascular Comorbidities in COPD.Antioxidants (Basel, Switzerland) · 2023Review
- Hypoxia Enhances Oxidative Stress in Neutrophils from ZZ Alpha-1 Antitrypsin Deficiency Patients.Antioxidants (Basel, Switzerland) · 2023Article
- LMAN1-MCFD2 complex is a cargo receptor for the ER-Golgi transport of α1-antitrypsin.The Biochemical journal · 2022Article
- The Mechanism of Mitochondrial Injury in Alpha-1 Antitrypsin Deficiency Mediated Liver Disease.International journal of molecular sciences · 2021Article
- Liver tumors in children with chronic liver diseases.World journal of gastrointestinal oncology · 2021Review
- Neuroserpin: structure, function, physiology and pathology.Cellular and molecular life sciences : CMLS · 2021Review
- Hepatocyte proteomes reveal the role of protein disulfide isomerase 4 in alpha 1-antitrypsin deficiency.JHEP reports : innovation in hepatology · 2021Article
- Oxidative Stress and Endoplasmic Reticulum Stress in Rare Respiratory Diseases.Journal of clinical medicine · 2021Review
- The Autophagy Pathway: A Critical Route in the Disposal of Alpha 1-Antitrypsin Aggregates That Holds Many Mysteries.International journal of molecular sciences · 2021Review
- Longitudinal Outcomes in Young Patients with Alpha-1-Antitrypsin Deficiency with Native Liver Reveal that Neonatal Cholestasis is a Poor Predictor of Future Portal Hypertension.The Journal of pediatrics · 2020Observational
- The Beneficial Effects of Antioxidants in Health And Diseases.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020Review
- Alpha-1 Antitrypsin Deficiency-Mediated Liver Toxicity: Why Do Some Patients Do Poorly? What Do We Know So Far?Chronic obstructive pulmonary diseases (Miami, Fla.) · 2020Review
- Article
- Greater survival despite increased complication rates following lung transplant for alpha-1-antitrypsin deficiency compared to chronic obstructive pulmonary disease.Journal of thoracic disease · 2019Article
- Pediatric hepatocellular carcinoma.World journal of gastroenterology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alpha-1-antitrypsin deficiency is a genetic disorder resulting in the expression of misfolded mutant protein that can polymerize and accumulate in hepatocytes, leading to liver disease in some individuals. Transgenic PiZ mice are a well-characterized model, which express human alpha-1-antitrypsin mutant Z protein (ATZ protein) and faithfully recapitulate the human liver disease. Liver tissue expressing alpha-1-antitrypsin mutant Z protein exhibits inflammation, injury and replacement of damaged cells. Fibrosis and hepatocellular carcinoma (HCC) develop in aging PiZ mice. In this study, microarray analysis was performed comparing young PiZ (ZY) mice to wild-type (WY), and indicated that there were alterations in gene expression levels that could influence a number of pathways leading to liver disease. Redox-regulating genes were up-regulated in ZY tissue, including carbonyl reductase 3 (CBR3), glutathione S-transferase alpha 1 + 2 (GSTA(1 + 2)) and glutathione S-transferase mu 3 (GSTM3). We hypothesized that oxidative stress could develop in Z mouse liver, contributing to tissue damage and disease progression with age. The results of biochemical analysis of PiZ mouse liver revealed that higher levels of reactive oxygen species (ROS) and a more oxidized, cellular redox state occurred in liver tissue from ZY mice than WY. ZY mice showed little evidence of oxidative cellular damage as assessed by protein carbonylation levels, malondialdehyde levels and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8oxodG) staining. Aging liver tissue from PiZ older mice (ZO) had elevated ROS, generally lower levels of antioxidant enzymes than younger mice and evidence of cellular damage. These data indicate that oxidative stress is a contributing factor in the development of liver disease in this model of alpha-1-antitrypsin deficiency.
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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.