ArticleExperimental & molecular medicine2022
Metabolic improvement and liver regeneration by inhibiting CXXC5 function for non-alcoholic steatohepatitis treatment.
Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- RYK is a GPNMB receptor that drives MASH.Nature · 2026Article
- Novel small molecules downregulate CDK1 expression and inhibit Wnt/β-catenin signaling in cutaneous squamous cell carcinoma by targeting its distinct tumor-specific cellular landscape.Experimental & molecular medicine · 2025Article
- CXXC5 function blockade promotes diabetic wound healing through stimulating fibroblast and vascular endothelial cell activation.Cell communication and signaling : CCS · 2025Article
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- Analysis of the Association Between TG/HDL, TyG, TyG-BMI, and ZJU Indices with Metabolic Dysfunction-Associated Fatty Liver Disease in Patients with Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Macrophage-tregs crosstalk: the "hub" of the immune network in MASLD.Frontiers in immunology · 2025Review
- Review
- Inhibiting the cytosolic function of CXXC5 accelerates diabetic wound healing by enhancing angiogenesis and skin repair.Experimental & molecular medicine · 2023Article
- Blockade of CXXC5-dishevelled interaction inhibits adipogenic differentiation, obesity, and insulin resistance in mice.Scientific reports · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-alcoholic steatohepatitis (NASH) is a chronic liver disease that results from multiple metabolic disorders. Considering the complexity of the pathogenesis, the identification of a factor mediating the multiple pathogenic phenotypes of NASH will be important for treatment. In this study, we found that CXXC5, a negative feedback regulator of the Wnt/β-catenin pathway, was overexpressed with suppression of Wnt/β-catenin signaling and its target genes involved in hepatic metabolism in obese-NASH patients. Cxxc5
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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 Socratic graph.