ArticleNature communications2018
AMPK activation counteracts cardiac hypertrophy by reducing O-GlcNAcylation.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers.
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Who cites it
165 citing papers in PubMed, 253 citations in OpenAlex.
- Transient elevation in cellular glucose uptake exacerbates pressure overload-induced cardiac hypertrophy and dysfunction.Epigenetics · 2026Article
- Glutamine Metabolism in Cardiac Hypertrophy.Reviews in cardiovascular medicine · 2026Review
- Tissue-specific expression and regulation of congenital disorders of glycosylation genes: A GTEx-based in silico study.Molecular genetics and metabolism reports · 2026Article
- PerturbingCells · 2026Article
- Osmolality-Independent Impact of Sodium on Glycosylation of an Fc-Fusion Protein and the Hexosamine Biosynthesis Pathway in a Chinese Hamster Ovary Cell Line.Biotechnology journal · 2026Article
- Myocardial metabolic remodeling in human end-stage ischemic and non-ischemic cardiomyopathy.Journal of molecular and cellular cardiology · 2026Article
- Sodium-myo-inositol cotransporter-1, SMIT1, promotes cardiac hypertrophy and fibrosis induced by pressure overload in mice.Cardiovascular research · 2026Article
- 1,1-Diethoxyethane enhances aerobic respiration in human mitochondria via activation of AMP-activated protein kinase.Communications biology · 2026Article
- MTFR1L is a cardiac antiaging factor for maintenance of mitochondrial homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Inhibiting SHP2 improves ventricular remodeling by restoring AMPK phosphorylation and mitochondrial homeostasis.Cell communication and signaling : CCS · 2026Article
- Functions of FGF21 and its role in cardiac hypertrophy.Journal of advanced research · 2026Review
- Pharmacological Foundation and Novel Insights of Resveratrol in Cardiovascular System: A Review.Current cardiology reviews · 2026Review
- Dysfunctional decidual CD2Frontiers in immunology · 2026Article
- Detection of cardiac O-GlcNAcylation via subcellular fractionation and dual antibody analysis in pressure overload cardiac hypertrophy.Glycobiology · 2025Article
- Glutamine: fructose-6-phosphate amidotransferase (GFAT) in the pathology of diseases: a review.Cell death discovery · 2025Review
- The impact of metformin on myocardial hypertrophy: an updated systematic review, meta-analysis, and meta-regression of randomized controlled trials.Diabetology & metabolic syndrome · 2025Review
- Article
- PFKFB2 Is Pivotal for Metabolic Flexibility and Differential Glucose Utilization.Journal of the American Heart Association · 2025Article
- Empagliflozin enhances metabolic efficiency and improves left ventricular hypertrophy in a hypertrophic cardiomyopathy mouse model.European heart journal · 2025Article
- Early Changes in Cardiac Macrophage Subsets in Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2025Article
105 more citing papers are in PubMed but not listed here.
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Authors and funding
21 authors at 7 institutions in 5 countries.
Funding
Abstract
AMP-activated protein kinase (AMPK) has been shown to inhibit cardiac hypertrophy. Here, we show that submaximal AMPK activation blocks cardiomyocyte hypertrophy without affecting downstream targets previously suggested to be involved, such as p70 ribosomal S6 protein kinase, calcineurin/nuclear factor of activated T cells (NFAT) and extracellular signal-regulated kinases. Instead, cardiomyocyte hypertrophy is accompanied by increased protein O-GlcNAcylation, which is reversed by AMPK activation. Decreasing O-GlcNAcylation by inhibitors of the glutamine:fructose-6-phosphate aminotransferase (GFAT), blocks cardiomyocyte hypertrophy, mimicking AMPK activation. Conversely, O-GlcNAcylation-inducing agents counteract the anti-hypertrophic effect of AMPK. In vivo, AMPK activation prevents myocardial hypertrophy and the concomitant rise of O-GlcNAcylation in wild-type but not in AMPKα2-deficient mice. Treatment of wild-type mice with O-GlcNAcylation-inducing agents reverses AMPK action. Finally, we demonstrate that AMPK inhibits O-GlcNAcylation by mainly controlling GFAT phosphorylation, thereby reducing O-GlcNAcylation of proteins such as troponin T. We conclude that AMPK activation prevents cardiac hypertrophy predominantly by inhibiting O-GlcNAcylation.
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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.