ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019
Reduced myocyte complex N-glycosylation causes dilated cardiomyopathy.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Genetic architecture of basal heart rate and its modulation by dietary salt in Drosophila melanogaster.PLoS genetics · 2026Article
- O-GlcNAcylation as a Metabolic Integrator in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2026Review
- Self-organizing network simulation of cardiac contraction dynamics.Chaos (Woodbury, N.Y.) · 2025Article
- N-acetylglucosaminyltransferase V attenuates myocardial infarction by mediating the insulin-like growth factor 1 receptor signaling pathway.Journal of translational internal medicine · 2025Article
- Integrated Multiomics Reveals Alterations in Paucimannose and Complex Type N-Glycans in Cardiac Tissue of Patients with COVID-19.Molecular & cellular proteomics : MCP · 2025Article
- Decoding glycosylation in cardiovascular diseases: mechanisms, biomarkers, and therapeutic opportunities.Frontiers in pharmacology · 2025Review
- Cardiomyocyte Reduction of Hybrid/Complex N-Glycosylation in the Adult Causes Heart Failure With Reduced Ejection Fraction in the Absence of Cellular Remodeling.Journal of the American Heart Association · 2024Article
- Protein glycosylation in cardiovascular health and disease.Nature reviews. Cardiology · 2024Review
- UGCG modulates heart hypertrophy through B4GalT5-mediated mitochondrial oxidative stress and the ERK signaling pathway.Cellular & molecular biology letters · 2023Article
- Reduced O-GlcNAcylation diminishes cardiomyocyte CaJournal of molecular and cellular cardiology · 2023Article
- miR-454-3p and miR-194-5p targeting cardiac sarcolemma ion exchange transcripts are potential noninvasive diagnostic biomarkers for childhood dilated cardiomyopathy in Egyptian patients.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2022Article
- Simulation Modeling of Reduced Glycosylation Effects on Potassium Channels of Mouse Cardiomyocytes.Frontiers in physiology · 2022Article
- Spatial N-glycomics of the human aortic valve in development and pediatric endstage congenital aortic valve stenosis.Journal of molecular and cellular cardiology · 2021Article
- An Overview of Glycosylation and its Impact on Cardiovascular Health and Disease.Frontiers in molecular biosciences · 2021Review
- Altered Glycosylation in the Aging Heart.Frontiers in molecular biosciences · 2021Article
- Intracellular O-linked glycosylation directly regulates cardiomyocyte L-type CaBasic research in cardiology · 2020Article
- A mutation in mannose-phosphate-dolichol utilization defect 1 reveals clinical symptoms of congenital disorders of glycosylation type I and dystroglycanopathy.JIMD reports · 2019Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Protein glycosylation is an essential posttranslational modification that affects a myriad of physiologic processes. Humans with genetic defects in glycosylation, which result in truncated glycans, often present with significant cardiac deficits. Acquired heart diseases and their associated risk factors were also linked to aberrant glycosylation, highlighting its importance in human cardiac disease. In both cases, the link between causation and corollary remains enigmatic. The glycosyltransferase gene, mannosyl (α-1,3-)-glycoprotein β-1,2- N-acetylglucosaminyltransferase (Mgat1), whose product, N-acetylglucosaminyltransferase 1 (GlcNAcT1) is necessary for the formation of hybrid and complex N-glycan structures in the medial Golgi, was shown to be at reduced levels in human end-stage cardiomyopathy, thus making Mgat1 an attractive target for investigating the role of hybrid/complex N-glycosylation in cardiac pathogenesis. Here, we created a cardiomyocyte-specific Mgat1 knockout (KO) mouse to establish a model useful in exploring the relationship between hybrid/complex N-glycosylation and cardiac function and disease. Biochemical and glycomic analyses showed that Mgat1KO cardiomyocytes produce predominately truncated N-glycan structures. All Mgat1KO mice died significantly younger than control mice and demonstrated chamber dilation and systolic dysfunction resembling human dilated cardiomyopathy (DCM). Data also indicate that a cardiomyocyte L-type voltage-gated Ca
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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 OpenQuestion graph.