ArticleCirculation2012
Carnitine palmitoyltransferase-1b deficiency aggravates pressure overload-induced cardiac hypertrophy caused by lipotoxicity.
Article in Circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers.
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Who cites it
131 citing papers in PubMed, 220 citations in OpenAlex.
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- Ethyl acetylsalicylate (E-ASA) protects against myocardial ischemia-reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- 20(S)-protopanaxatriol ameliorates cardiac hypertrophy by activating the AMPK/PGC-1α/PPARγ signaling pathway.Journal of ginseng research · 2026Article
- CPT1B K321 crotonylation contributes to cardiac dysfunction in endotoxic shock.Experimental & molecular medicine · 2026Article
- Semaglutide augments vascular proliferation and cardiac performance in a large animal model of ischemic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2026Article
- Investigation of potential sex-based differences in trastuzumab-induced chronic cardiotoxicity in a rat model.Frontiers in pharmacology · 2026Article
- Metabolic reprogramming in cardiac fibrosis: mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- [Overwork damages myocardial energy metabolism homeostasis in mice].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Myocardial lipin1 protects the heart against ischemic injury by preserving lipid homeostasis.JCI insight · 2025Article
- The impact of lipid metabolism on ferroptosis in myocardial ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2025Review
- Metabolic-Electrophysiological Coupling in Heart Failure: from Bidirectional Decoupling to Therapeutic Recoupling.Current heart failure reports · 2025Review
- Novel therapeutic strategies for targeting fatty acid oxidation in cancer.Biomarker research · 2025Review
- Systemic Metabolic Rewiring in a Mouse Model of Left Ventricular Hypertrophy.International journal of molecular sciences · 2025Article
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- AAV-mediated overexpression of CPT1B protects from cardiac hypertrophy and heart failure in a murine pressure overload model.Basic research in cardiology · 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
- Dietary Insulinogenic Amino Acid Restriction Improves Glucose Metabolism in a Neonatal Piglet Model.Nutrients · 2025Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCarnitine palmitoyltransferase-1 (CPT1) is a rate-limiting step of mitochondrial β-oxidation by controlling the mitochondrial uptake of long-chain acyl-CoAs. The muscle isoform, CPT1b, is the predominant isoform expressed in the heart. It has been suggested that inhibiting CPT1 activity by specific CPT1 inhibitors exerts protective effects against cardiac hypertrophy and heart failure. However, clinical and animal studies have shown mixed results, thereby creating concerns about the safety of this class of drugs. Preclinical studies using genetically modified animal models should provide a better understanding of targeting CPT1 to evaluate it as a safe and effective therapeutic approach. METHODS AND
resultsHeterozygous CPT1b knockout (CPT1b(+/-)) mice were subjected to transverse aorta constriction-induced pressure overload. These mice showed overtly normal cardiac structure/function under the basal condition. Under a severe pressure-overload condition induced by 2 weeks of transverse aorta constriction, CPT1b(+/-) mice were susceptible to premature death with congestive heart failure. Under a milder pressure-overload condition, CPT1b(+/-) mice exhibited exacerbated cardiac hypertrophy and remodeling compared with wild-type littermates. There were more pronounced impairments of cardiac contraction with greater eccentric cardiac hypertrophy in CPT1b(+/-) mice than in control mice. Moreover, the CPT1b(+/-) heart exhibited exacerbated mitochondrial abnormalities and myocardial lipid accumulation with elevated triglycerides and ceramide content, leading to greater cardiomyocyte apoptosis.
conclusionsCPT1b deficiency can cause lipotoxicity in the heart under pathological stress, leading to exacerbation of cardiac pathology. Therefore, caution should be exercised in the clinical use of CPT1 inhibitors.
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What OpenQuestion holds
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.