ArticleEMBO molecular medicine2014
Metabolic crosstalk between the heart and liver impacts familial hypertrophic cardiomyopathy.
Article in EMBO molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 46 citations in OpenAlex.
- Heart-derived factors and organ cross-talk in settings of health and disease: new knowledge and clinical opportunities for multimorbidity.The Journal of physiology · 2026Review
- Systemic Metabolic Rewiring in a Mouse Model of Left Ventricular Hypertrophy.International journal of molecular sciences · 2025Article
- Association of liver fibrosis-4 index with adverse outcomes in hypertrophic cardiomyopathy patients.ESC heart failure · 2024Article
- The Multifaceted Roles of Macrophages in NAFLD Pathogenesis.Cellular and molecular gastroenterology and hepatology · 2023Review
- Targeting lipid metabolism as a new therapeutic strategy for inherited cardiomyopathies.Frontiers in cardiovascular medicine · 2023Review
- Whole-Exome Sequencing Revealed New Candidate Genes for Human Dilated Cardiomyopathy.Diagnostics (Basel, Switzerland) · 2022Article
- Machine learning and bioinformatics to identify 8 autophagy-related biomarkers and construct gene regulatory networks in dilated cardiomyopathy.Scientific reports · 2022Article
- Burmese pythons exhibit a transient adaptation to nutrient overload that prevents liver damage.The Journal of general physiology · 2022Article
- The role of CD36 in cardiovascular disease.Cardiovascular research · 2022Review
- Dysfunctional Network and Mutation Genes of Hypertrophic Cardiomyopathy.Journal of healthcare engineering · 2022Article
- Atrial Lesions in a Pedigree WithFrontiers in cardiovascular medicine · 2022Article
- Plasma metabolomic profiling of hypertrophic cardiomyopathy patients before and after surgical myectomy suggests postoperative improvement in metabolic function.BMC cardiovascular disorders · 2021Article
- Human-induced pluripotent stem cells for modelling metabolic perturbations and impaired bioenergetics underlying cardiomyopathies.Cardiovascular research · 2021Review
- Hepatocardiac or Cardiohepatic Interaction: From Traditional Chinese Medicine to Western Medicine.Evidence-based complementary and alternative medicine : eCAM · 2021Review
- Pharmacokinetic and Biochemical Profiling of Sodium Dichloroacetate in Pregnant Ewes and Fetuses.Drug metabolism and disposition: the biological fate of chemicals · 2020Article
- Metabolic Alterations in Inherited Cardiomyopathies.Journal of clinical medicine · 2019Review
- Cardiac myocyte KLF5 regulates body weight via alteration of cardiac FGF21.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Hypertrophic Cardiomyopathy: A Vicious Cycle Triggered by Sarcomere Mutations and Secondary Disease Hits.Antioxidants & redox signaling · 2019Review
- Protective Effect of Lactobacillus rhamnosus GG and its Supernatant against Myocardial Dysfunction in Obese Mice Exposed to Intermittent Hypoxia is Associated with the Activation of Nrf2 Pathway.International journal of biological sciences · 2019Article
- Liver-specific rescuing of CEACAM1 reverses endothelial and cardiovascular abnormalities in male mice with null deletion of Ceacam1 gene.Molecular metabolism · 2018Article
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2 authors at 1 institution in 1 country.
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Abstract
Familial hypertrophic cardiomyopathy (HCM) is largely caused by dominant mutations in genes encoding cardiac sarcomeric proteins, and it is etiologically distinct from secondary cardiomyopathies resulting from pressure/volume overload and neurohormonal or inflammatory stimuli. Here, we demonstrate that decreased left ventricular contractile function in male, but not female, HCM mice is associated with reduced fatty acid translocase (CD36) and AMP-activated protein kinase (AMPK) activity. As a result, the levels of myocardial ATP and triglyceride (TG) content are reduced, while the levels of oleic acid and TG in circulating very low density lipoproteins (VLDLs) and liver are increased. With time, these metabolic changes culminate in enhanced glucose production in male HCM mice. Remarkably, restoration of ventricular TG and ATP deficits via AMPK agonism as well as inhibition of gluconeogenesis improves ventricular architecture and function. These data underscore the importance of the systemic effects of a primary genetic heart disease to other organs and provide insight into potentially novel therapeutic interventions for HCM.
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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.