ArticleClinical and molecular hepatology2024
DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease.
Article in Clinical and molecular hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Integrative multi-omics analysis identifies stellate cell-derived complement component 7 as a predictor of fibrosis and liver-related events in MASLD.JHEP reports : innovation in hepatology · 2026Article
- DNMT1 facilitates the progression of metabolic dysfunction-associated steatotic liver disease by impeding transcription mediated by HNF4α and PPARα.Clinical and molecular hepatology · 2026Article
- Diagnostic innovation and models of care to improve fibrosis detection and risk stratification in steatotic liver disease.The Lancet regional health. Europe · 2026Review
- Multi-Target Intervention of Traditional Chinese Medicine in Metabolic Dysfunction-Associated Steatohepatitis: Comprehensive Treatment Strategies from Lipotoxicity to Immune Regulation.International journal of general medicine · 2026Review
- Gut microbiota and the gut-liver axis in MASLD: mechanisms, immune regulation and therapeutic opportunities.Frontiers in pharmacology · 2026Review
- Viral manipulation of host cell glutamine metabolism and glutamine rewiring in hepatic diseases: Editorial on "Glutamate dehydrogenase 1-dependent α-ketoglutarate promotes hepatitis B virus transcription by modulating histone methylations on the covalently closed circular DNA minichromosome".Clinical and molecular hepatology · 2026Article
- Panomics in metabolic dysfunction-associated steatotic liver disease: unravelling the drivers of disease heterogeneity.Clinical and molecular hepatology · 2026Review
- Transcriptional and epigenetic regulation of CaBioinformatics advances · 2026Article
- Exposure-shaped immunometabolic networks in chronic liver disease: translating multi-omics and artificial intelligence into preventive biomarkers.Frontiers in immunology · 2026Review
- Gradual DNA methylation changes reveal transcription factors implicated in metabolic dysfunction-associated steatotic liver disease progression and epigenetic age acceleration.Clinical epigenetics · 2025Article
- Sepsis-related immune signature C3 in endometrial carcinoma: implications for prognosis, tumor progression through bioinformatics and experimental validation.Molecular biology reports · 2025Article
- A complement to epigenetics in metabolic dysfunction-associated steatotic liver disease: Editorial on "DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease".Clinical and molecular hepatology · 2025Article
- Correspondence to editorial on "DNA methylome analysis reveals epigenetic alteration of complement genes in advanced metabolic dysfunction-associated steatotic liver disease".Clinical and molecular hepatology · 2025Article
- Role of genetic variants and DNA methylation of lipid metabolism-related genes in metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2025Review
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Authors and funding
15 authors.
Funding
Abstract
BACKGROUND/
aimsBlocking the complement system is a promising strategy to impede the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the interplay between complement and MASLD remains to be elucidated. This comprehensive approach aimed to investigate the potential association between complement dysregulation and the histological severity of MASLD.
methodsLiver biopsy specimens were procured from a cohort comprising 106 Korean individuals, which included 31 controls, 17 with isolated steatosis, and 58 with metabolic dysfunction-associated steatohepatitis (MASH). Utilizing the Infinium Methylation EPIC array, thorough analysis of methylation alterations in 61 complement genes was conducted. The expression and methylation of nine complement genes in a murine MASH model were examined using quantitative RT-PCR and pyrosequencing.
resultsMethylome and transcriptome analyses of liver biopsies revealed significant (P<0.05) hypermethylation and downregulation of C1R, C1S, C3, C6, C4BPA, and SERPING1, as well as hypomethylation (P<0.0005) and upregulation (P<0.05) of C5AR1, C7, and CD59, in association with the histological severity of MASLD. Furthermore, DNA methylation and the relative expression of nine complement genes in a MASH diet mouse model aligned with human data.
conclusionOur research provides compelling evidence that epigenetic alterations in complement genes correlate with MASLD severity, offering valuable insights into the mechanisms driving MASLD progression, and suggests that inhibiting the function of certain complement proteins may be a promising strategy for managing MASLD.
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