ArticleModern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc2019
Detection of DNA damage response in nonalcoholic fatty liver disease via p53-binding protein 1 nuclear expression.
Article in Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 33 citations in OpenAlex.
- Significance of p53-binding protein 1 as an in situ DNA damage marker for ulcerative colitis.Medical molecular morphology · 2026Article
- Facilitated DNA damage repair as an emerging therapeutic strategy for inflammatory and fibrotic diseases.RSC chemical biology · 2026Review
- Involvement of Activin E depletion in metabolic dysfunction-associated steatohepatitis.Biochemistry and biophysics reports · 2025Article
- Early alternative splicing signatures and RBP networks in MASLD progression to cirrhosis.BMC medical genomics · 2025Article
- Exposure to low levels of hexavalent chromium in drinking water alters diet-induced steatotic liver disease in male rats.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2025Article
- Liver, ageing and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- ACMSD inhibition corrects fibrosis, inflammation, and DNA damage in MASLD/MASH.Journal of hepatology · 2025Article
- DNA sensors in metabolic and cardiovascular diseases: Molecular mechanisms and therapeutic prospects.Immunological reviews · 2025Review
- Roles of chromatin and genome instability in cellular senescence and their relevance to ageing and related diseases.Nature reviews. Molecular cell biology · 2024Review
- Macrophages and T cells in metabolic disorder-associated cancers.Nature reviews. Cancer · 2024Review
- Transcriptomic Landscape Analysis Reveals a Persistent DNA Damage Response in Metabolic Dysfunction-associated Steatohepatitis Post-dietary Intervention.Journal of clinical and translational hepatology · 2024Article
- Significance of P53-Binding Protein 1 as a Novel Molecular Histological Marker for Hypopharyngeal Squamous Neoplasms.Cancers · 2024Article
- Long-term prognosis and DNA damage status after oral mucosal epithelial cell sheet transplantation following esophageal endoscopic submucosal dissection for squamous cell carcinoma: A case series.Regenerative therapy · 2024Article
- Dietary intervention reverses molecular markers of hepatocellular senescence in the GAN diet-induced obese and biopsy-confirmed mouse model of NASH.BMC gastroenterology · 2024Article
- Review
- Mitochondrial Impairment: A Link for Inflammatory Responses Activation in the Cardiorenal Syndrome Type 4.International journal of molecular sciences · 2023Review
- Single-Nucleotide Polymorphisms in Base-Excision Repair-Related Genes Involved in the Risk of an Occurrence of Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2023Article
- MiR-182-5p Is Upregulated in Hepatic Tissues from a Diet-Induced NAFLD/NASH/HCC C57BL/6J Mouse Model and Modulates Cyld and Foxo1 Expression.International journal of molecular sciences · 2023Article
- Impaired fatty acid metabolism perpetuates lipotoxicity along the transition to chronic kidney injury.JCI insight · 2022Article
- Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2022Review
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease is a major liver disease that leads to cirrhosis and/or hepatocellular carcinoma in a subset of patients. The mechanism underlying disease progression is largely unknown. p53-binding protein 1 (53BP1) is a DNA damage response protein that rapidly localizes at the site of DNA double-strand breaks. In this study, we investigated nuclear 53BP1-positive foci formation as an indicator of DNA double-strand breaks in human nonalcoholic fatty liver disease liver tissues by immunofluorescence microscopy. A total of 52 liver tissue samples, including 43 nonalcoholic fatty liver disease samples and 9 controls, were studied. Our results show that the number of abnormal 53BP1-positive foci in hepatocytes (defined as three or more discrete nuclear foci and/or large foci greater than 1 μM) was significantly increased in nonalcoholic fatty liver disease patients compared to that in controls, both in nonalcoholic fatty liver (p < 0.01) and nonalcoholic steatohepatitis patients (p < 0.01). The number of large foci was significantly increased in the nonalcoholic steatohepatitis cases compared to that in the nonalcoholic fatty liver cases (p < 0.05) and correlated with increased stage of fibrosis. The number of large-foci-expressing hepatocytes was positively correlated with increased age (p < 0.01) and negatively correlated with serum platelet count (p < 0.05). In addition, we performed an in vitro assay using rat hepatocytes treated with the saturated free fatty acid palmitate. Treatment appeared to augment the number of abnormal foci, indicating an induction of double-strand breaks in the hepatocytes through free fatty acid treatment in a caspase-dependent manner. This study demonstrates that 53BP1-positive nuclear foci formation is associated with disease progression in nonalcoholic fatty liver disease patients. Analysis of 53BP1 expression might be a feasible technique to estimate genomic instability in nonalcoholic fatty liver disease.
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