ArticleCardiovascular research2015
AMPK deficiency in cardiac muscle results in dilated cardiomyopathy in the absence of changes in energy metabolism.
Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Metabolic remodeling of substrate utilization during heart failure progression.Heart failure reviews · 2019Pooled it
- Metabolic Task Analysis Reveals Distinct Metabotypes in End-Stage Dilated Cardiomyopathy.Circulation. Genomic and precision medicine · 2026Article
- Sevoflurane induces developmental cardiotoxicity via AMPKα2 dysregulation in zebrafish.Cell & bioscience · 2026Article
- Isoform-specific roles of AMP-activated protein kinase in cardiac physiology and pathophysiology.Frontiers in cardiovascular medicine · 2025Review
- Traditional Chinese Medicine Treating Dilated Cardiomyopathy: A Literature Review.International journal of general medicine · 2025Review
- Review
- Role of sestrins in metabolic and aging-related diseases.Biogerontology · 2024Review
- Inhibition of PRKAA/AMPK (Ser485/491) phosphorylation by crizotinib induces cardiotoxicity via perturbing autophagosome-lysosome fusion.Autophagy · 2024Article
- Anti-Diabetic Therapy and Heart Failure: Recent Advances in Clinical Evidence and Molecular Mechanism.Life (Basel, Switzerland) · 2023Review
- The Protective Effect of 11-Keto-β-Boswellic Acid against Diabetic Cardiomyopathy in Rats Entails Activation of AMPK.Nutrients · 2023Article
- Review
- Cardiovascular protection by SGLT2 inhibitors - Do anti-inflammatory mechanisms play a role?Molecular metabolism · 2022Review
- AMPK deficiency in smooth muscles causes persistent pulmonary hypertension of the new-born and premature death.Nature communications · 2022Article
- Impaired AMP-Activated Protein Kinase Signaling in Heart Failure With Preserved Ejection Fraction-Associated Atrial Fibrillation.Circulation · 2022Article
- Spatiotemporal AMPKα2 deletion in mice induces cardiac dysfunction, fibrosis and cardiolipin remodeling associated with mitochondrial dysfunction in males only.Biology of sex differences · 2021Article
- Role of Cardiac AMP-Activated Protein Kinase in a Non-pathological Setting: Evidence From Cardiomyocyte-Specific, Inducible AMP-Activated Protein Kinase α1α2-Knockout Mice.Frontiers in cell and developmental biology · 2021Article
- AMPKβ1 and AMPKβ2 define an isoform-specific gene signature in human pluripotent stem cells, differentially mediating cardiac lineage specification.The Journal of biological chemistry · 2020Article
- Nutritional modulation of heart failure in mitochondrial pyruvate carrier-deficient mice.Nature metabolism · 2020Article
- Longevity genes, cardiac ageing, and the pathogenesis of cardiomyopathy: implications for understanding the effects of current and future treatments for heart failure.European heart journal · 2020Article
- Molecular, Cellular, and Clinical Evidence That Sodium-Glucose Cotransporter 2 Inhibitors Act as Neurohormonal Antagonists When Used for the Treatment of Chronic Heart Failure.Journal of the American Heart Association · 2020Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
Abstract
aimsAMP-activated protein kinase (AMPK) is thought to be a central player in regulating myocardial metabolism and its activation has been shown to inhibit cardiac hypertrophy. Recently, mice with muscle-specific deletion of AMPK β1/β2 subunits (AMPKβ1β2-deficient mice, β1β2M-KO) have been generated and possess <10% of normal AMPK activity in muscle. However, how/if dramatic AMPK deficiency alters cardiac metabolism, function, or morphology has not been investigated. Therefore, the aim of this study was to determine whether a significant loss of AMPK activity alters cardiac function, metabolism, and hypertrophy, and whether this may play a role in the pathogenesis of heart failure. METHODS AND
resultsβ1β2M-KO mice exhibit an approximate 25% reduction in systolic and diastolic function compared with wild-type (WT) littermates. Despite the well-documented role of AMPK in controlling myocardial energy metabolism, there was no difference in basal glucose and fatty acid oxidation rates between β1β2M-KO and WT mice. However, there was reduced AMPK-mediated phosphorylation of troponin I in β1β2M-KO and reduced ventricular cell shortening in the presence of low Ca(2+), which may explain the impaired cardiac function in these mice. Interestingly, β1β2M-KO mice did not display any signs of compensatory cardiac hypertrophy, which could be attributed to impaired activation of p38 MAPK.
conclusionsβ1β2M-KO mice display evidence of dilated cardiomyopathy. This is the first mouse model of AMPK deficiency that demonstrates cardiac dysfunction in the absence of pathological stress and provides insights into the role of AMPK in regulating myocardial function, metabolism, hypertrophy, and the progression to heart failure.
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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.