ArticleMolecular metabolism2019
Mapping the molecular signatures of diet-induced NASH and its regulation by the hepatokine Tsukushi.
Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
58 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Key hepatic signatures of human and mouse nonalcoholic steatohepatitis: A transcriptome-proteome data meta-analysis.Frontiers in endocrinology · 2022Pooled it
- Revealing the Shared Genetic Architecture of Metabolic Dysfunction-Associated Steatotic Liver Disease-Related Traits Through Genomic Structural Equation Modeling.Genetic epidemiology · 2026Article
- Hepatic FXR deficiency exacerbates dyslipidemia by disrupting the gut-liver axis via bile acid disorder and gut microbiota dysbiosis.Journal of translational medicine · 2026Article
- A comparison of plasma Tsukushi in adolescents with and without metabolic dysfunction-associated steatotic liver disease.Physiological reports · 2026Article
- Hepatic GPR110 contributes to sex disparity in the development of MASH through oestrogen receptor α-dependent signalling.Nature metabolism · 2026Article
- YTHDC1 Is Essential for Postnatal Liver Development and Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Myeloid TGF-β signaling shapes liver macrophage heterogeneity and metabolic liver disease pathogenesis.JHEP reports : innovation in hepatology · 2025Article
- Serum Tsukushi level is negatively associated with cholesterol efflux capacity in metabolic dysfunction-associated steatotic liver disease: a cross-sectional study.Scientific reports · 2025Article
- p53 and TIGAR promote redox control to protect against metabolic dysfunction-associated steatohepatitis.JHEP reports : innovation in hepatology · 2025Article
- Autocrine GDF10 Inhibits Hepatic Stellate Cell Activation via BMPR2/ALK3 Receptor to Prevent Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Brain-acting hepatokines: its impact on energy balance and metabolism.Frontiers in neuroscience · 2025Review
- Hepatokines and MASLD: The GLP1-Ras-FGF21-Fetuin-A Crosstalk as a Therapeutic Target.International journal of molecular sciences · 2024Review
- Transcriptome Analyses of Liver Sinusoidal Endothelial Cells Reveal a Consistent List of Candidate Genes Associated with Endothelial Dysfunction and the Fibrosis Progression.Current issues in molecular biology · 2024Article
- Emerging Insights into the Role of BDNF on Health and Disease in Periphery.Biomolecules · 2024Review
- Geroprotective interventions converge on gene expression programs of reduced inflammation and restored fatty acid metabolism.GeroScience · 2024Article
- Hepatic danger signaling triggers TREM2Science translational medicine · 2024Article
- Transcriptomics-driven metabolic pathway analysis reveals similar alterations in lipid metabolism in mouse MASH model and human.Communications medicine · 2024Article
- Unraveling the cGAS/STING signaling mechanism: impact on glycerolipid metabolism and diseases.Frontiers in medicine · 2024Review
- Molecular and cellular mechanisms underlying the hepatoprotective role of ghrelin against NAFLD progression.Journal of physiology and biochemistry · 2023Review
- Combination of an ACLY inhibitor with a GLP-1R agonist exerts additive benefits on nonalcoholic steatohepatitis and hepatic fibrosis in mice.Cell reports. Medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveNonalcoholic steatohepatitis (NASH) is closely associated with metabolic syndrome and increases the risk for end-stage liver disease, such as cirrhosis and hepatocellular carcinoma. Despite this, the molecular events that influence NASH pathogenesis remain poorly understood. The objectives of the current study are to delineate the transcriptomic and proteomic signatures of NASH liver, to identify potential pathogenic pathways and factors, and to critically assess their role in NASH pathogenesis.
methodsWe performed RNA sequencing and quantitative proteomic analyses on the livers from healthy and diet-induced NASH mice. We examined the association between plasma levels of TSK, a newly discovered hepatokine, and NASH pathologies and reversal in response to dietary switch in mice. Using TSK knockout mouse model, we determined how TSK deficiency modulates key aspects of NASH pathogenesis.
resultsRNA sequencing and quantitative proteomic analyses revealed that diet-induced NASH triggers concordant reprogramming of the liver transcriptome and proteome in mice. NASH pathogenesis is linked to elevated plasma levels of the hepatokine TSK, whereas dietary switch reverses NASH pathologies and reduces circulating TSK concentrations. Finally, TSK inactivation protects mice from diet-induced NASH and liver transcriptome remodeling.
conclusionsGlobal transcriptomic and proteomic profiling of healthy and NASH livers revealed the molecular signatures of diet-induced NASH and dysregulation of the liver secretome. Our study illustrates a novel pathogenic mechanism through which elevated TSK in circulation promotes NASH pathologies, thereby revealing a potential target for therapeutic intervention.
Indexed as
Identifiers
What 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.