ArticleJHEP reports : innovation in hepatology2026
Enhanced lysosomal glycogen breakdown is associated with liver tumorigenesis in glycogen storage disease type III.
Article in JHEP reports : innovation in hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Pathological depositions in human disease: converging mechanisms in atherosclerosis, Alzheimer's disease, and related disorders.Molecular biomedicine · 2026Review
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27 authors.
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Abstract
Background & Aims: Glycogen storage disease type III (GSDIII) is a rare metabolic disorder caused by mutations in the glycogen debranching enzyme ( Methods: Liver and tumor samples from 14-month-old Results: Conclusions: In GSDIII, liver metabolism is characterized by the accumulation of structurally abnormal glycogen and a significant reduction of key energy substrates. In this metabolic context, enhanced lysosomal glycogen degradation may support tumor growth, highlighting a mechanistic link between glycogen metabolism and the development of liver cancer. Impact and implications: This study provides novel insights into the metabolic dysregulations driving liver tumorigenesis in glycogen storage disease type III (GSDIII). Our findings reveal a potential link between abnormal glycogen accumulation and liver cancer, highlighting the pivotal role of lysosomal glycogen degradation in supporting tumor growth. These results are particularly important for researchers and clinicians working on metabolic liver diseases, as they suggest potential glycogen-targeting therapeutic strategies for GSDIII and other related liver disorders. Practically, they could guide future interventions aimed at modulating glycogen metabolism, offering new treatment avenues for patients with GSDIII at risk of hepatocellular carcinoma, while contributing to the broader understanding of metabolic dysregulation in cancer biology.
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