ArticleLipids2017
AMPK Prevents Palmitic Acid-Induced Apoptosis and Lipid Accumulation in Cardiomyocytes.
Article in Lipids, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
- Cardamonin activates AMPK/FOXO3a/Nrf-2 axis to ameliorate oxidative stress in hyperlipidemia induced cardiac injury in mice.Molecular biology reports · 2026Article
- Cellular basis of HFpEF: contributions of abnormal lipids.Frontiers in cardiovascular medicine · 2026Review
- The regulatory role of exercise in heart failure and myocardial energy metabolism: A review.Biomolecules & biomedicine · 2025Review
- Comprehensive Analysis of Metabolic Changes in Mice Exposed to Corilagin Based on GC-MS Analysis.Drug design, development and therapy · 2025Article
- The potential of herbal drugs to treat heart failure: The roles of Sirt1/AMPK.Journal of pharmaceutical analysis · 2024Review
- Suppression of the gut microbiota-bile acid-FGF19 axis in patients with atrial fibrillation.Cell proliferation · 2023Article
- Cardiac lipid metabolism, mitochondrial function, and heart failure.Cardiovascular research · 2023Review
- Fetal metabolic adaptations to cardiovascular stress in twin-twin transfusion syndrome.iScience · 2023Article
- SGLT2 inhibitors: role in protective reprogramming of cardiac nutrient transport and metabolism.Nature reviews. Cardiology · 2023Review
- ATF4-mediated CD36 upregulation contributes to palmitate-induced lipotoxicity in hepatocytes.American journal of physiology. Gastrointestinal and liver physiology · 2023Article
- L-carnitine attenuated hyperuricemia-associated left ventricular remodeling through ameliorating cardiomyocytic lipid deposition.Frontiers in pharmacology · 2023Article
- Pharmacological inhibition of adipose tissue adipose triglyceride lipase by Atglistatin prevents catecholamine-induced myocardial damage.Cardiovascular research · 2022Article
- The role of CD36 in cardiovascular disease.Cardiovascular research · 2022Review
- Metabolomic Profiling of Brain Protective Effect of Edaravone on Cerebral Ischemia-Reperfusion Injury in Mice.Frontiers in pharmacology · 2022Article
- Soluble epoxide hydrolase deficiency attenuates lipotoxic cardiomyopathy via upregulation of AMPK-mTORC mediated autophagy.Journal of molecular and cellular cardiology · 2021Article
- Molecular Mechanism of Palmitic Acid on Myocardial Contractility in Hypertensive Rats and Its Relationship with Neural Nitric Oxide Synthase Protein in Cardiomyocytes.BioMed research international · 2021Article
- Hepatitis C virus nonstructural protein 5A perturbs lipid metabolism by modulating AMPK/SREBP-1c signaling.Lipids in health and disease · 2019Article
- Skeletal muscle miR-34a/SIRT1:AMPK axis is activated in experimental and human non-alcoholic steatohepatitis.Journal of molecular medicine (Berlin, Germany) · 2019Article
- CD36 mediates lipid accumulation in pancreatic beta cells under the duress of glucolipotoxic conditions: Novel roles of lysine deacetylases.Biochemical and biophysical research communications · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Palmitic acid, a main fatty acid (FA) in human nutrition, can induce apoptosis of cardiomyocytes. However, a specific combination of palmitic, myristic and palmitoleic acid (CoFA) has been reported to promote beneficial cardiac growth. The aim of this study was to investigate the relevance of CoFA for cardiac growth and to delineate the underlying signaling pathways of CoFA and palmitic acid treatment. CoFA treatment of C57Bl/6 mice increased FA serum concentrations. However, morphologic and echocardiographic analysis did not show myocardial hypertrophy. Cell culture studies using rat ventricular cardiomyocytes revealed an increased phosphorylation of AMP activated protein kinase α (AMPKα) to 155 ± 19% and its target acetyl-CoA-carboxylase to 177 ± 23% by CoFA. Treatment with myristic acid also increased AMPKα phosphorylation to 189 ± 32%. Palmitic acid did not activate AMPKα but increased expression of the FA translocase CD36 (FAT/CD36) to 163 ± 23% and adipose-differentiation-related-protein (ADRP), a sensitive marker of lipid accumulation, to 168 ± 42%. This was associated with an increased phosphorylation of the stress-activated-protein-kinase/Jun-amino-terminal-kinase (SAPK/JNK) to 173 ± 27%. In CoFA-treated cells, phosphorylation of SAPK/JNK was unaltered. FACS analysis revealed increased apoptosis to 159 ± 5% by palmitic acid but not by CoFA. AMPK activator AICAR (5-aminoimidazole-4-carboxamide ribonucleotide) prevented up-regulation of ADRP and increased apoptosis by palmitic acid. Confirming these findings, inhibition of AMPK by compound C in CoFA-treated cardiomyocytes resulted in an increased expression of ADRP to 154 ± 27%, FAT/CD36 to 167 ± 28% and apoptosis to 183 ± 12%. These data reveal that AMPK activation plays an important role in prevention of palmitic acid-induced apoptosis and lipid accumulation in cardiomyocytes.
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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.