ArticleAging cell2025
Aging-Associated Liver Sinusoidal Endothelial Cells Dysfunction Aggravates the Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Mechanometabolic endothelial senescence as a translational framework for cardiometabolic vascular disease and vascular ageing.Molecular biology reports · 2026Review
- Dietary, Nutrient, and Supramolecular Nanofiber Modulation of the Liver Sinusoidal Clearance System in Metabolic Diseases and Aging.Biomedicines · 2026Review
- The Sphingolipid Balance and Endothelial Dysfunction in Lysosomal Storage Diseases: Shared Mechanisms in Gaucher, Niemann-Pick and Fabry Disease.International journal of molecular sciences · 2026Review
- [Research progress on cellular senescence and liver diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Review
- The Interplay Between Cellular Senescence and Lipid Metabolism in the Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).International journal of molecular sciences · 2026Review
- Key Experimental Therapeutics and Knowledge Gaps in Metabolic Dysfunction-Associated Steatohepatitis (MASH).Drug design, development and therapy · 2026Review
- Diversity of oxidative stress and senescence phenotypes induced by chemotherapeutic agents in HUVECs.Scientific reports · 2025Article
- Liver, ageing and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- Exploring hepatic stellate cell-driven fibrosis: therapeutic advances and future perspectives.ADMET & DMPK · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Aging increases the susceptibility to metabolic dysfunction-associated steatotic liver disease (MASLD). Liver sinusoidal endothelial cells (LSECs) help in maintaining hepatic homeostasis, but the contribution of age-associated LSECs dysfunction to MASLD is not clear. The aim of this study was to investigate the effect of aging-associated LSECs dysfunction on MASLD. Free fatty acid-treated AML12 cells were co-cultured with young and etoposide-induced senescent TSEC cells to evaluate the senescence-associated endothelial effects on the lipid accumulation in hepatocytes. In addition, young and aged rats were subjected to methionine-choline-deficient diet-induced metabolic dysfunction-associated steatohepatitis (MASH). Hepatic hemodynamics and endothelial dysfunction were evaluated by in situ liver perfusion. Liver tissue samples from young and aged healthy controls and MASH patients were also analyzed. Steatotic AML12 cells co-cultured with young TSEC cells showed less lipid accumulation, and such effect was abolished by eNOS inhibitor or with senescent TSEC cells. However, co-culture with resveratrol-treated senescent TSEC cells could partially resume the NO-mediated protective effects of endothelial cells. Furthermore, aged MASH rats showed more severe liver injury, steatosis, fibrosis, and endothelial and microcirculatory dysfunction. In addition, aged MASH patients showed more pronounced liver injury and fibrosis with lower hepatic eNOS, p-eNOS, and SIRT1 protein levels than in young patients. Senescence compromises the protective effects of LSECs against hepatocyte steatosis. In addition, aging aggravates not only liver steatosis and fibrosis but also intensifies LSECs dysfunction in MASH rats. Accordingly aged MASH patients also showed endothelial dysfunction with more severe liver injury and fibrosis.
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