ArticleJournal of cellular and molecular medicine2020
Inhibition of CPT2 exacerbates cardiac dysfunction and inflammation in experimental endotoxaemia.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Lipid dysregulation in mouse ovarian antral follicles after oral exposure to a human relevant mixture of three phthalates.Toxicology · 2026Article
- Gut microbiota: new links between exercise and disease.Frontiers in microbiology · 2026Review
- NFIA regulates articular chondrocyte fatty acid metabolism and joint homeostasis.Science translational medicine · 2025Article
- Myocardial pyruvate dehydrogenase kinase 4 drives sex-specific cardiac responses to endotoxemia.JCI insight · 2025Article
- Dietary L-carnitine modulates oxidative stress, lipid metabolism, and pulmonary hypertension in chickens raised at high-altitude under cold stress.BMC veterinary research · 2025Article
- Mendelian randomization demonstrates a causal link between peripheral circulating acylcarnitines and intracranial aneurysms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Sirt5 improves cardiomyocytes fatty acid metabolism and ameliorates cardiac lipotoxicity in diabetic cardiomyopathy via CPT2 de-succinylation.Redox biology · 2024Article
- Intestinal Flora: A Potential New Regulator of Cardiovascular Disease.Aging and disease · 2022Review
- Protective Effects of Meldonium in Experimental Models of Cardiovascular Complications with a Potential Application in COVID-19.International journal of molecular sciences · 2021Article
- Long-Chain Acyl-Carnitines Interfere with Mitochondrial ATP Production Leading to Cardiac Dysfunction in Zebrafish.International journal of molecular sciences · 2021Article
- The role and therapeutic implication of CPTs in fatty acid oxidation and cancers progression.American journal of cancer research · 2021Review
- Carnitine Palmitoyltransferase System: A New Target for Anti-Inflammatory and Anticancer Therapy?Frontiers in pharmacology · 2021Review
- Inhibition of CPT2 exacerbates cardiac dysfunction and inflammation in experimental endotoxaemia.Journal of cellular and molecular medicine · 2020Article
- Microbiota-Derived Metabolite Trimethylamine N-Oxide Protects Mitochondrial Energy Metabolism and Cardiac Functionality in a Rat Model of Right Ventricle Heart Failure.Frontiers in cell and developmental biology · 2020Article
- Gut microbiota-palmitoleic acid-interleukin-5 axis orchestrates benzene-induced hematopoietic toxicity.Gut microbesArticle
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The suppression of energy metabolism is one of cornerstones of cardiac dysfunction in sepsis/endotoxaemia. To investigate the role of fatty acid oxidation (FAO) in the progression of inflammation-induced cardiac dysfunction, we compared the effects of FAO-targeting compounds on mitochondrial and cardiac function in an experimental model of lipopolysaccharide (LPS)-induced endotoxaemia. In LPS-treated mice, endotoxaemia-induced inflammation significantly decreased cardiac FAO and increased pyruvate metabolism, while cardiac mechanical function was decreased. AMP-activated protein kinase activation by A769662 improved mitochondrial FAO without affecting cardiac function and inflammation-related gene expression during endotoxaemia. Fatty acid synthase inhibition by C75 restored both cardiac and mitochondrial FAO; however, no effects on inflammation-related gene expression and cardiac function were observed. In addition, the inhibition of carnitine palmitoyltransferase 2 (CPT2)-dependent FAO by aminocarnitine resulted in the accumulation of FAO intermediates, long-chain acylcarnitines, in the heart. As a result, cardiac pyruvate metabolism was inhibited, which further exacerbated inflammation-induced cardiac dysfunction. In conclusion, although inhibition of CPT2-dependent FAO is detrimental to cardiac function during endotoxaemia, present findings show that the restoration of cardiac FAO alone is not sufficient to recover cardiac function. Rescue of cardiac FAO should be combined with anti-inflammatory therapy to ameliorate cardiac dysfunction in endotoxaemia.
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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.