ArticleScientific reports2025
Histone methyltransferase SMYD2 regulates the activation of hepatic stellate cells by activating TLR4 signaling.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- Targeting SMYD2 improves immunotherapy response in experimental hepatocellular carcinoma.Molecular therapy. Oncology · 2026Article
- Olive (Olea europaea) phenolics for the control of psoriasis via targeting SMYD2 and IL-17A protein-protein interaction networks.Journal of natural medicines · 2026Article
- The role of histone methylation in fibrosis and its therapeutic potential.Journal of translational medicine · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
Liver fibrosis represents a pathological outcome in the progression of chronic liver diseases, primarily driven by the activation of hepatic stellate cells (HSCs) induced by various chronic liver injury factors. Substantial evidence indicates that under inflammatory conditions, aberrant activation of HSCs leads to excessive deposition of extracellular matrix (ECM). Therefore, identifying novel molecular targets to inhibit HSCs activation and proliferation is of significant clinical importance for the prevention and treatment of liver fibrosis. SMYD2 (SET and MYND domain containing 2) is a histone methyltransferase primarily responsible for catalyzing the methylation of lysine 36 on histone H3 (H3K36). However, the specific role and mechanisms of SMYD2 in the progression of liver fibrosis remain poorly understood. Thus, this study aims to systematically investigate the molecular regulatory mechanisms of SMYD2 in the development of liver fibrosis. Our findings demonstrate that both SMYD2 and its catalytic product, H3K36me2, are significantly upregulated in carbon tetrachloride (CCl
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