ArticleFibrogenesis & tissue repair2016
Age-dependent development of liver fibrosis in Glmp (gt/gt) mice.
Article in Fibrogenesis & tissue repair, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed.
- GLMP promotes EGFR-TKI resistance by activating autophagy and RhoA pathway in non-small cell lung cancer.NPJ precision oncology · 2025Article
- Cathepsin D is essential for the degradomic shift of macrophages required to resolve liver fibrosis.Molecular metabolism · 2024Article
- Regulatory T-cell deficiency leads to features of autoimmune liver disease overlap syndrome in scurfy mice.Frontiers in immunology · 2023Article
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- Common Transcriptional Program of Liver Fibrosis in Mouse Genetic Models and Humans.International journal of molecular sciences · 2021Article
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Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMice lacking glycosylated lysosomal membrane protein (Glmp (gt/gt) mice) have liver fibrosis as the predominant phenotype due to chronic liver injury. The Glmp (gt/gt) mice grow and reproduce at the same rate as their wild-type siblings. Life expectancy is around 18 months.
methodsWild-type and Glmp (gt/gt) mice were studied between 1 week and 18 months of age. Livers were analyzed using histological, immunohistochemical, biochemical, and qPCR analyses.
resultsIt was shown that Glmp (gt/gt) mice were not born with liver injury; however, it appeared shortly after birth as indicated by excess collagen expression, deposition of fibrous collagen in the periportal areas, and increased levels of hydroxyproline in Glmp (gt/gt) liver. Liver functional tests indicated a chronic, mild liver injury. Markers of inflammation, fibrosis, apoptosis, and modulation of extracellular matrix increased from an early age, peaking around 4 months of age and followed by attenuation of these signals. To compensate for loss of hepatocytes, the oval cell compartment was activated, with the highest activity of the oval cells detected at 3 months of age, suggesting insufficient hepatocyte proliferation in Glmp (gt/gt) mice around this age. Although constant proliferation of hepatocytes and oval cells maintained adequate hepatic function in Glmp (gt/gt) mice, it also resulted in a higher frequency of liver tumors in older animals.
conclusionsThe Glmp (gt/gt) mouse is proposed as a model for slowly progressing liver fibrosis and possibly as a model for a yet undescribed human lysosomal disorder.
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Registered trials
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