ArticleHepatology (Baltimore, Md.)2020
hnRNPU/TrkB Defines a Chromatin Accessibility Checkpoint for Liver Injury and Nonalcoholic Steatohepatitis Pathogenesis.
Article in Hepatology (Baltimore, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 46 citations in OpenAlex.
- The Cardio-Renal-Hepatic Axis in MASLD. Role of BDNF, NGF, and Metabolic Cross-Talk.Current hypertension reports · 2026Review
- Hepatocyte TrkB Acts as a Gatekeeper Against MASH-Related Liver Fibrosis by Suppressing the TGFβ/CCL2 Axis and Macrophage Infiltration.Cell proliferation · 2026Article
- SLC13A2-transported citrate remodels transcriptional regulation through protein acetylation to suppress tumor growth.Science advances · 2026Article
- Review of roles of RNA-binding proteins on NAFLD and the related pharmaceutical measures.Biomolecules & biomedicine · 2025Review
- SLC13A2 promotes hepatocyte metabolic remodeling and liver regeneration by enhancing de novo cholesterol biosynthesis.The EMBO journal · 2025Article
- Effect of Multiyear Biodegradable Plastic Mulch on Soil Microbial Community, Assembly, and Functioning.Microorganisms · 2025Article
- Alternative splicing: hallmark and therapeutic opportunity in metabolic liver disease.Gastroenterology report · 2025Review
- Chromatin accessibility: biological functions, molecular mechanisms and therapeutic application.Signal transduction and targeted therapy · 2024Review
- Review
- The impact of magnesium biotinate and arginine silicate complexes on metabolic dysfunctions, antioxidant activity, inflammation, and neuromodulation in high-fat diet-fed rats.Clinical and experimental medicine · 2024Article
- Myokines: metabolic regulation in obesity and type 2 diabetes.Life metabolism · 2024Review
- TM7SF3 controls TEAD1 splicing to prevent MASH-induced liver fibrosis.Cell metabolism · 2024Article
- Emerging Insights into the Role of BDNF on Health and Disease in Periphery.Biomolecules · 2024Review
- CitrusNutrients · 2024Article
- AGXT2 Suppresses the Proliferation and Dissemination of Hepatocellular Carcinoma Cells by Modulating Intracellular Lipid Metabolism.Journal of hepatocellular carcinoma · 2024Article
- Deficiency of the Heterogeneous Nuclear Ribonucleoprotein U locus leads to delayed hindbrain neurogenesis.Biology open · 2023Article
- Article
- p38-mediated FOXN3 phosphorylation modulates lung inflammation and injury through the NF-κB signaling pathway.Nucleic acids research · 2023Article
- Review
- Targeting HNRNPU to overcome cisplatin resistance in bladder cancer.Molecular cancer · 2022Article
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
BACKGROUND AND
aimsNonalcoholic steatohepatitis (NASH) is a progressive liver disease that is characterized by liver injury, inflammation, and fibrosis. NASH pathogenesis is linked to reprogramming of chromatin landscape in the liver that predisposes hepatocytes to stress-induced tissue injury. However, the molecular nature of the putative checkpoint that maintains chromatin architecture and preserves hepatocyte health remains elusive. APPROACH AND
resultsHere we show that heterogeneous nuclear ribonucleoprotein U (hnRNPU), a nuclear matrix protein that governs chromatin architecture and gene transcription, is a critical factor that couples chromatin disruption to NASH pathogenesis. RNA-seq and chromatin immunoprecipitation-seq studies revealed an extensive overlap between hnRNPU occupancy and altered gene expression during NASH. Hepatocyte-specific inactivation of hnRNPU disrupted liver chromatin accessibility, activated molecular signature of NASH, and sensitized mice to diet-induced NASH pathogenesis. Mechanistically, hnRNPU deficiency stimulated the expression of a truncated isoform of TrkB (TRKB-T1) that promotes inflammatory signaling in hepatocytes and stress-induced cell death. Brain-derived neurotrophic factor treatment reduced membrane TRKB-T1 protein and protected mice from diet-induced NASH.
conclusionsThese findings illustrate a mechanism through which disruptions of chromatin architecture drive the emergence of disease-specific signaling patterns that promote liver injury and exacerbate NASH pathogenesis.
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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.