ArticleESC heart failure2025
Pathogenic glycosyltransferase genes and potential therapeutic drugs in pressure overload-induced heart failure.
Article in ESC heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- DC-FusionGNN: A Dual-Channel Framework Integrating Global Self-Attention and Local Topology Learning for Identifying Key Resistance Genes AgainstPlants (Basel, Switzerland) · 2026Article
- A gene interaction network-based molecular taxonomy of dilated cardiomyopathy highlighting immune and inflammatory heterogeneity.Clinical and experimental medicine · 2026Article
- Pathogenic glycosyltransferase genes and potential therapeutic drugs in pressure overload-induced heart failure.ESC heart failure · 2025Article
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Authors and funding
6 authors.
Funding
Abstract
aimsProtein glycosylation regulated by glycosyltransferases is an important type of post-translational modification. The role of the glycosyltransferase genes (GTGs) in heart failure (HF) remains unclear and requires further investigation.
methodsDifferential expression analysis was performed on the transverse aortic constriction (TAC)-related dataset GSE36074 to screen out the differentially expressed GTGs. Enrichment and protein-protein interaction analyses explored their functional mechanisms and interconnections. Pearson correlation analysis revealed the relationship between GTGs and pathological cardiac remodelling. The upstream miRNAs of GTGs were predicted using corresponding online databases, and the downstream target genes were identified by weighted correlation network analysis (WGCNA). Computer virtual screening and molecular docking predicted potential therapeutic drugs. The identified GTGs were validated in vivo, in vitro and in the human HF-related dataset GSE57338.
resultsTwenty-one differentially expressed GTGs were identified, and these genes were significantly up-regulated in the TAC model except for C1galt1, Extl2 and Pigh. Pearson correlation analysis revealed that 11 GTGs were significantly associated with pathological cardiac remodelling. Fifty-six miRNAs and 31 drugs were predicted to target these GTGs. WGCNA indicated that these GTGs were associated with lipid metabolism-related genes and pathways. Up-regulation of B3gnt9, C1galt1, Gcnt1, Gxylt2 and Mgat5b was observed in the TAC model. GXYLT2 is up-regulated and has high disease-predictive value in patients with dilated cardiomyopathy and ischaemic cardiomyopathy. Knockdown of GXYLT2 in human AC16 cardiomyocytes significantly attenuated angiotensin II (AngII)-induced hypertrophy.
conclusionsDysregulation of GTG expression may affect TAC-induced HF through metabolic pathways, and GXYLT2 may be a new potential therapeutic target for HF.
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