ArticleAmerican journal of cancer research2016
Lack of fibroblast growth factor 21 accelerates metabolic liver injury characterized by steatohepatities in mice.
Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- Aberrant lipid metabolism renders an aggressive behavior of T-lymphoblastic lymphoma in a MASH model.Oncogene · 2026Article
- FGF21 deletion mildly exacerbates hepatic dysfunction in GAN diet and alcohol fed rats.npj metabolic health and disease · 2025Article
- Overexpression of LSR suppresses glioma proliferation and invasion via regulating FOXO3a.Journal of neuro-oncology · 2025Article
- Reversion of metabolic dysfunction-associated steatohepatitis by skeletal muscle-directed FGF21 gene therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- PPIH as a poor prognostic factor increases cell proliferation and m6A RNA methylation in hepatocellular carcinoma.American journal of cancer research · 2024Article
- Noninvasive biomarkers in pediatric nonalcoholic fatty liver disease.World journal of hepatology · 2023Review
- Fibroblast Growth Factor-21 as a Potential Therapeutic Target of Nonalcoholic Fatty Liver Disease.Therapeutics and clinical risk management · 2023Review
- Lipid metabolism in tumor microenvironment: novel therapeutic targets.Cancer cell international · 2022Review
- Hepatocyte-specific fibroblast growth factor 21 overexpression ameliorates high-fat diet-induced obesity and liver steatosis in mice.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Article
- The potential function and clinical application of FGF21 in metabolic diseases.Frontiers in pharmacology · 2022Review
- The role of FGF21 and its analogs on liver associated diseases.Frontiers in medicine · 2022Review
- T Cell Subsets and Natural Killer Cells in the Pathogenesis of Nonalcoholic Fatty Liver Disease.International journal of molecular sciences · 2021Review
- Non-Alcoholic Steatohepatitis Severity Associates with FGF21 Level and Kidney Glucose Uptake.Metabolic syndrome and related disorders · 2021Article
- Bile acid activated receptors: Integrating immune and metabolic regulation in non-alcoholic fatty liver disease.Liver research (Beijing, China) · 2021Review
- FGF21 in obesity and cancer: New insights.Cancer letters · 2021Review
- Pancreatic Tumorigenesis: Oncogenic KRAS and the Vulnerability of the Pancreas to Obesity.Cancers · 2021Review
- Aberrant FGFR4 signaling worsens nonalcoholic steatohepatitis in FGF21KO mice.International journal of biological sciences · 2021Article
- Advances of Fibroblast Growth Factor/Receptor Signaling Pathway in Hepatocellular Carcinoma and its Pharmacotherapeutic Targets.Frontiers in pharmacology · 2021Review
- High fat diet, gut microbiome and gastrointestinal cancer.Theranostics · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor 21 (FGF21) concentrations are increased in human subjects who either have type 2 diabetes or nonalcoholic fatty liver disease (NAFLD). While excessive fat in the liver promotes the release of pro-inflammatory cytokines, NAFLD progresses from steatosis to non alcoholic steatohepatitis (NASH), a more aggressive form of hepatic damage, and lastly toward cirrhosis and HCC. In our previous study, loss of FGF21 is associated with hyper-proliferation, aberrant p53, and HCC development in diabetes mice. In this study, we proposed to investigate the liver metabolic disorders by diabetes and the potential roles of FGF21 played in NASH and potential carcinogenetic transformation of HCC. NASH was induced in FGF21 knockout (FGF21KO) mice by streptozotocin administration or fed with high fat diet (HFD). The pathological transformation of steatohepatities as well as parameters of inflammation, lipid metabolism, cellular events, mesenchymal-epithelial transition (MET) and Wnt/β-catenin signaling was determined in the FGF21 KO diabetic mice and HFD fed mice. We found that mice lacking the FGF21 gene are more prone to develop NASH. A compromised microenvironment of NASH, which could facilitate the HCC carcinogenetic transformation, was found in FGF21 KO mice under metabolic disorders by diabetes and HFD feeding. This study provided further evidence that lack of FGF21 worsened the metabolic disorders in NASH and could render a tumor microenvironment for HCC initiation and progression in the liver of diabetes mice.
Indexed as
Identifiers
27293995PMC4889716W2473806208What OpenQuestion holds
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.