ArticleThe Journal of clinical investigation2000
Deactivation of peroxisome proliferator-activated receptor-alpha during cardiac hypertrophic growth.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 183 papers.
What it found
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Who cites it
183 citing papers in PubMed, 459 citations in OpenAlex.
- PPARalpha gene variation and physical performance in Russian athletes.European journal of applied physiology · 2006Trial
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- Histone Deacetylase 7 protects against pathologic cardiac hypertrophy.Journal of molecular and cellular cardiology · 2026Article
- Cardiac Lipid Metabolism: Cells, Metabolites, and Rhythms.Circulation research · 2026Review
- Peroxisome proliferator-activated receptor-α activation attenuates susceptibility to postoperative atrial fibrillation.Journal of thoracic disease · 2026Article
- Dihydromyricetin confers protection against myocardial ischemia-reperfusion injury by inhibiting ferroptosis through direct targeting of PPARα.Frontiers in pharmacology · 2026Article
- Mitochondrial remodeling in heart failure with reduced ejection fraction.Frontiers in physiology · 2026Review
- MiR-199a family members are differentially regulated during physiological and pathological cardiac hypertrophy.Frontiers in physiology · 2026Article
- Inflammation in cardiovascular-kidney-metabolic syndrome: key roles and underlying mechanisms-a comprehensive review.Molecular and cellular biochemistry · 2025Review
- Peroxisome Proliferator-Activated Receptor Family of Lipid-Activated Nuclear Receptors Alpha Silencing Promotes Oxidative Stress and Hypertrophic Phenotype in Rat Cardiac Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Signaling and transcriptional dynamics underlying early adaptation to oncogenic BRAF inhibition.Cell systems · 2025Article
- Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025Review
- Herbal Insights: Exploring the Therapeutic Potential of Indian Dietary Herbs in Diabetic Cardiomyopathy Management.Current diabetes reviews · 2025Review
- Raising NADCirculation · 2023Article
- Role of STIM1 in the Regulation of Cardiac Energy Substrate Preference.International journal of molecular sciences · 2023Review
- The Janus-Faced Role of Lipid Droplets in Aging: Insights from the Cellular Perspective.Biomolecules · 2023Review
- Integrated Control of Fatty Acid Metabolism in Heart Failure.Metabolites · 2023Review
- Targeting Mitochondrial Metabolism to Save the Failing Heart.Life (Basel, Switzerland) · 2023Review
- Metabolic landscape in cardiac aging: insights into molecular biology and therapeutic implications.Signal transduction and targeted therapy · 2023Review
- Low-carbohydrate diets containing plant-derived fat but not animal-derived fat ameliorate heart failure.Scientific reports · 2023Article
123 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
We sought to delineate the molecular regulatory events involved in the energy substrate preference switch from fatty acids to glucose during cardiac hypertrophic growth. alpha(1)-adrenergic agonist-induced hypertrophy of cardiac myocytes in culture resulted in a significant decrease in palmitate oxidation rates and a reduction in the expression of the gene encoding muscle carnitine palmitoyltransferase I (M-CPT I), an enzyme involved in mitochondrial fatty acid uptake. Cardiac myocyte transfection studies demonstrated that M-CPT I promoter activity is repressed during cardiac myocyte hypertrophic growth, an effect that mapped to a peroxisome proliferator-activated receptor-alpha (PPARalpha) response element. Ventricular pressure overload studies in mice, together with PPARalpha overexpression studies in cardiac myocytes, demonstrated that, during hypertrophic growth, cardiac PPARalpha gene expression falls and its activity is altered at the posttranscriptional level via the extracellular signal-regulated kinase mitogen-activated protein kinase pathway. Hypertrophied myocytes exhibited reduced capacity for cellular lipid homeostasis, as evidenced by intracellular fat accumulation in response to oleate loading. These results indicate that during cardiac hypertrophic growth, PPARalpha is deactivated at several levels, leading to diminished capacity for myocardial lipid and energy homeostasis.
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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.