ArticlePloS one2016
A New Mouse Model That Spontaneously Develops Chronic Liver Inflammation and Fibrosis.
Article in PloS one, 2016. 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, 15 citations in OpenAlex.
- Harmonizing mouse anatomy terminology: a common language?Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Structure-function analysis of time-resolved immunological phases in metabolic dysfunction-associated fatty liver disease (MASH) comparing the NIF mouse model to human MASH.Scientific reports · 2024Article
- Prospect of Animal Models for Acute-on-chronic Liver Failure: A Mini-review.Journal of clinical and translational hepatology · 2022Review
- Environmental allergens house dust mite-induced asthma is associated with ferroptosis in the lungs.Experimental and therapeutic medicine · 2021Article
- Animal and Organoid Models of Liver Fibrosis.Frontiers in physiology · 2021Review
- NKT cells promote both type 1 and type 2 inflammatory responses in a mouse model of liver fibrosis.Scientific reports · 2020Article
- The Roles of Immune Cells in the Pathogenesis of Fibrosis.International journal of molecular sciences · 2020Review
- Single cell RNA-seq reveals profound transcriptional similarity between Barrett's oesophagus and oesophageal submucosal glands.Nature communications · 2018Article
- The immunomodulatory quinoline-3-carboxamide paquinimod reverses established fibrosis in a novel mouse model for liver fibrosis.PloS one · 2018Article
- Surgical and immune reconstitution murine models in bone marrow research: Potential for exploring mechanisms in sepsis, trauma and allergy.World journal of experimental medicine · 2017Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here we characterize a new animal model that spontaneously develops chronic inflammation and fibrosis in multiple organs, the non-obese diabetic inflammation and fibrosis (N-IF) mouse. In the liver, the N-IF mouse displays inflammation and fibrosis particularly evident around portal tracts and central veins and accompanied with evidence of abnormal intrahepatic bile ducts. The extensive cellular infiltration consists mainly of macrophages, granulocytes, particularly eosinophils, and mast cells. This inflammatory syndrome is mediated by a transgenic population of natural killer T cells (NKT) induced in an immunodeficient NOD genetic background. The disease is transferrable to immunodeficient recipients, while polyclonal T cells from unaffected syngeneic donors can inhibit the disease phenotype. Because of the fibrotic component, early on-set, spontaneous nature and reproducibility, this novel mouse model provides a unique tool to gain further insight into the underlying mechanisms mediating transformation of chronic inflammation into fibrosis and to evaluate intervention protocols for treating conditions of fibrotic disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.