ArticleHepatology (Baltimore, Md.)2016
Mutant p53 in concert with an interleukin-27 receptor alpha deficiency causes spontaneous liver inflammation, fibrosis, and steatosis in mice.
Article in Hepatology (Baltimore, Md.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Profiling of extracellular vesicles from primary hepatocytes, organoids, and mash patients identifies cell injury-specific signatures.Scientific reports · 2026Article
- Chronic High-Fat Diet Does Not Alter Overall Cancer Incidence in Trp53R270H/+ Mice.Cancer research communications · 2026Article
- Network pharmacology, molecular docking, molecular dynamics simulation, and in vivo experiments elucidate the potential mechanisms of berberine against liver injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Potential therapeutic strategies for MASH: from preclinical to clinical development.Life metabolism · 2024Review
- p53R245W Mutation Fuels Cancer Initiation and Metastases in NASH-driven Liver Tumorigenesis.Cancer research communications · 2023Article
- Protective Effects ofInternational journal of molecular sciences · 2023Article
- Inflammation suppresses DLG2 expression decreasing inflammasome formation.Journal of cancer research and clinical oncology · 2022Article
- Targeted therapeutics and novel signaling pathways in non-alcohol-associated fatty liver/steatohepatitis (NAFL/NASH).Signal transduction and targeted therapy · 2022Review
- IL27 Signaling Serves as an Immunologic Checkpoint for Innate Cytotoxic Cells to Promote Hepatocellular Carcinoma.Cancer discovery · 2022Article
- The role of p53 in liver fibrosis.Frontiers in pharmacology · 2022Review
- Study on mechanism of matrine in treatment of COVID-19 combined with liver injury by network pharmacology and molecular docking technology.Drug delivery · 2021Article
- Metabolic Reprogramming of Colorectal Cancer Cells and the Microenvironment: Implication for Therapy.International journal of molecular sciences · 2021Review
- WSX1 act as a tumor suppressor in hepatocellular carcinoma by downregulating neoplastic PD-L1 expression.Nature communications · 2021Article
- Characterization With KRAS Mutant Is a Critical Determinant in Immunotherapy and Other Multiple Therapies for Non-Small Cell Lung Cancer.Frontiers in oncology · 2021Review
- Silencing of functional p53 attenuates NAFLD by promoting HMGB1-related autophagy induction.Hepatology international · 2020Article
- Exploring the Emerging Role of the Gut Microbiota and Tumor Microenvironment in Cancer Immunotherapy.Frontiers in immunology · 2020Review
- Endothelin-1 differentially directs lineage specification of adipose- and bone marrow-derived mesenchymal stem cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Control of metabolism by p53 - Cancer and beyond.Biochimica et biophysica acta. Reviews on cancer · 2018Review
- Role of nonresolving inflammation in hepatocellular carcinoma development and progression.NPJ precision oncology · 2018Review
- Immunomodulatory Function of the Tumor Suppressor p53 in Host Immune Response and the Tumor Microenvironment.International journal of molecular sciences · 2016Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledThe cellular and molecular etiology of unresolved chronic liver inflammation remains obscure. Whereas mutant p53 has gain-of-function properties in tumors, the role of this protein in liver inflammation is unknown. Herein, mutant p53(R172H) is mechanistically linked to spontaneous and sustained liver inflammation and steatosis when combined with the absence of interleukin-27 (IL27) signaling (IL27RA), resembling the phenotype observed in nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) patients. Indeed, these mice develop, with age, hepatocyte necrosis, immune cell infiltration, fibrosis, and micro- and macrosteatosis; however, these phenotypes are absent in mutant p53(R172H) or IL27RA(-/-) mice. Mechanistically, endothelin A receptor (ETAR)-positive macrophages are highly accumulated in the inflamed liver, and chemical inhibition of ETAR signaling reverses the observed phenotype and negatively regulates mutant p53 levels in macrophages.
conclusionThe combination of mutant p53 and IL27RA(-/-) causes spontaneous liver inflammation, steatosis, and fibrosis in vivo, whereas either gene alone in vivo has no effects on the liver.
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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.