ArticleThe journals of gerontology. Series A, Biological sciences and medical sciences2014
Liver aging and pseudocapillarization in a Werner syndrome mouse model.
Article in The journals of gerontology. Series A, Biological sciences and medical sciences, 2014. 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.
- Review
- Microvascular Health as a Key Determinant of Organismal Aging.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- The impact of aging on liver health and the development of liver diseases.Hepatology communications · 2025Review
- Aging and metabolic dysfunction-associated steatotic liver disease: a bidirectional relationship.Frontiers of medicine · 2025Review
- The relationship between spontaneous cystic degeneration and pseudocapillarization in sinusoids in the liver of aged Sprague-Dawley rats.Journal of toxicologic pathology · 2025Article
- Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
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- Stress-Induced Premature Senescence Related to Oxidative Stress in the Developmental Programming of Nonalcoholic Fatty Liver Disease in a Rat Model of Intrauterine Growth Restriction.Antioxidants (Basel, Switzerland) · 2022Article
- The multifaceted roles of DNA repair and replication proteins in aging and obesity.DNA repair · 2021Review
- Sirtuin 1 ameliorates defenestration in hepatic sinusoidal endothelial cells during liver fibrosis via inhibiting stress-induced premature senescence.Cell proliferation · 2021Article
- Crosstalk among DNA Damage, Mitochondrial Dysfunction, Impaired Mitophagy, Stem Cell Attrition, and Senescence in the Accelerated Ageing Disorder Werner Syndrome.Cytogenetic and genome research · 2021Review
- A glitch in the matrix: Age-dependent changes in the extracellular matrix facilitate common sites of metastasis.Aging and cancer · 2020Article
- Review
- LSEC model of aging.Aging · 2020Article
- New aspects of hepatic endothelial cells in physiology and nonalcoholic fatty liver disease.American journal of physiology. Cell physiology · 2020Review
- Supraphysiological protection from replication stress does not extend mammalian lifespan.Aging · 2020Article
- Aging-Related Molecular Pathways in Chronic Cholestatic Conditions.Frontiers in medicine · 2019Review
- Hallmarks of Aging in the Liver.Computational and structural biotechnology journal · 2019Review
- Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Werner syndrome is a progeric syndrome characterized by premature atherosclerosis, diabetes, cancer, and death in humans. The knockout mouse model created by deletion of the RecQ helicase domain of the mouse Wrn homologue gene (Wrn(∆hel/∆hel)) is of great interest because it develops atherosclerosis and hypertriglyceridemia, conditions associated with aging liver and sinusoidal changes. Here, we show that Wrn(∆hel/∆hel) mice exhibit increased extracellular matrix, defenestration, decreased fenestration diameter, and changes in markers of liver sinusoidal endothelial cell inflammation, consistent with age-related pseudocapilliarization. In addition, hepatocytes are larger, have increased lipofuscin deposition, more frequent nuclear morphological anomalies, decreased mitochondria number, and increased mitochondrial diameter compared to wild-type mice. The Wrn(∆hel/∆hel) mice also have altered mitochondrial function and altered nuclei. Microarray data revealed that the Wrn(∆hel/∆hel) genotype does not affect the expression of many genes within the isolated hepatocytes or liver sinusoidal endothelial cells. This study reveals that Wrn(∆hel/∆hel) mice have accelerated typical age-related liver changes including pseudocapillarization. This confirms that pseudocapillarization of the liver sinusoid is a consistent feature of various aging models. Moreover, it implies that DNA repair may be implicated in normal aging changes in the liver.
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