ArticleJournal of translational internal medicine2025
N-acetylglucosaminyltransferase V attenuates myocardial infarction by mediating the insulin-like growth factor 1 receptor signaling pathway.
Article in Journal of translational internal medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- The impact of pericardial disruption on heart function and remodeling after myocardial infarction in mice.The international journal of cardiovascular imaging · 2026Article
- Harnessing Ribonucleoprotein Granule Biology for Cancer Therapy: The Central Role of Protein Modifications.Research (Washington, D.C.) · 2026Review
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Authors and funding
9 authors.
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Abstract
Background and Objectives: N-glycosylation, a crucial post-translational modification, is well-recognized for its pivotal role in cardiovascular functions. N-acetylglucosaminyltransferase V (GnT-V) is one of the major glycosyltransferases that determine the complexity of N-glycans in N-glycosylation modification. This study aimed to explore the role of GnT-V in myocardial infarction (MI). Methods: Proteomics and N-glycoproteomic analysis were performed on myocardial tissues for the N-glycosylation profile after MI. Adeno-associated virus (AAV) with a mouse cTnT promoter was utilized to induce overexpression of GnT-V in the heart for the role of GnT-V in MI. Echocardiography and histological analysis were used to evaluate the effect of GnT-V on MI. For the potential mechanisms of GnT-V, proteomic analysis was performed on cardiomyocytes that were subjected to GnT-V overexpression and hypoxic stress. The results were validated by western blot, lectin blot and immunoprecipitation assays, and confirmed with PNGase F and tunicamycin treatment. Results: N-glycosylation of protein was significantly reduced after MI, which could be related to a decrease in the expression levels of GnT-V and its target glycans. Targeted GnT-V overexpression in the heart by using AAV improved cardiac function and reduced the infarct size after MI. Further, proteomics analysis of cardiomyocytes revealed that insulin-like growth factor-binding protein 3 (IGFBP3) was targeted by GnT-V and induced degradation through the lysosome pathway. Consequently, the insulin-like growth factor 1 receptor (IGF1R) signaling pathway was activated through overexpression of GnT-V. Conclusion: Our findings suggest that promoting the IGF1R signaling cascades by regulating the N-glycosylation of certain proteins in the signaling pathway, especially through GnT-V, may act as a promising strategy for treating MI.
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