ArticleJournal of the American Heart Association2019
O-GlcNAc Transferase Promotes Compensated Cardiac Function and Protein Kinase A O-GlcNAcylation During Early and Established Pathological Hypertrophy From Pressure Overload.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Novel Quality Metrics for Assessing the Reproducibility and Translational Relevance of Mouse Transverse Aortic Constriction Experiments: A Systematic Review.Journal of the American Heart Association · 2026Pooled it
- O-GlcNAcylation: A bridge for regulating the function of the "heart-kidney-bone axis".Biochemistry and biophysics reports · 2026Review
- Metabo-epigenetic circuits of heart failure: chromatin-modifying enzymes as determinants of metabolic plasticity.EMBO molecular medicine · 2026Review
- Detection of cardiac O-GlcNAcylation via subcellular fractionation and dual antibody analysis in pressure overload cardiac hypertrophy.Glycobiology · 2025Article
- OGT-mediated O-GlcNAc of FOXO1 promotes the progression of neonatal heart failure via regulating pyroptosis.Scientific reports · 2025Article
- Sex alters thyroid hormone's effect on protein O-GlcNAcylation in the aged mouse heart.BMC molecular and cell biology · 2025Article
- Protein glycosylation in cardiovascular health and disease.Nature reviews. Cardiology · 2024Review
- Roles of O-GlcNAcylation in Mitochondrial Homeostasis and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Sustained Increases in Cardiomyocyte ProteinJournal of the American Heart Association · 2023Article
- Best practices in assessing cardiac proteinAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- Exercise, exerkines, and cardiometabolic health: from individual players to a team sport.The Journal of clinical investigation · 2023Review
- Article
- Review
- Role of Posttranslational Modifications of Proteins in Cardiovascular Disease.Oxidative medicine and cellular longevity · 2022Review
- First comprehensive identification of cardiac proteins with putative increased O-GlcNAc levels during pressure overload hypertrophy.PloS one · 2022Article
- The dual role of the hexosamine biosynthetic pathway in cardiac physiology and pathophysiology.Frontiers in endocrinology · 2022Review
- Article
- Cardiomyocyte protein O-GlcNAcylation is regulated by GFAT1 not GFAT2.Biochemical and biophysical research communications · 2021Article
- Temporal regulation of protein O-GlcNAc levels during pressure-overload cardiac hypertrophy.Physiological reports · 2021Article
- Role ofPhysiological reviews · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Background Protein posttranslational modifications by O-linked β-N-acetylglucosamine (O-GlcNAc) increase with cardiac hypertrophy, yet the functional effects of these changes are incompletely understood. In other organs, O-GlcNAc promotes adaptation to acute physiological stressors; however, prolonged O-GlcNAc elevations are believed to be detrimental. We hypothesize that early O-GlcNAcylation improves cardiac function during initial response to pressure overload hypertrophy, but that sustained elevations during established pathological hypertrophy negatively impact cardiac function by adversely affecting calcium handling proteins. Methods and Results Transverse aortic constriction or sham surgeries were performed on littermate controls or cardiac-specific, inducible O-GlcNAc transferase knockout (OGTKO) mice to reduce O-GlcNAc levels. O-GlcNAc transferase deficiency was induced at different times. To evaluate the initial response to pressure overload, OGTKO was completed preoperatively and mice were followed for 2 weeks post-surgery. To assess prolonged O-GlcNAcylation during established hypertrophy, OGTKO was performed starting 18 days after surgery and mice were followed until 6 weeks post-surgery. In both groups, OGTKO with transverse aortic constriction caused significant left ventricular dysfunction. OGTKO did not affect levels of the calcium handling protein SERCA2a. OGTKO reduced phosphorylation of phospholamban and cardiac troponin I, which would negatively impact cardiac function. O-GlcNAcylation of protein kinase A catalytic subunit, a kinase for phospholamban, decreased with OGTKO. Conclusions O-GlcNAcylation promotes compensated cardiac function in both early and established pathological hypertrophy. We identified a novel O-GlcNAcylation of protein kinase A catalytic subunit, which may regulate calcium handling and cardiac function.
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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.