ArticleCell reports. Medicine2025
Targeting long-chain acylcarnitine accumulation to protect cardiac mitochondrial homeostasis after complete revascularization.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- An oral-gut microbial metabolite linksGut microbes · 2026Article
- Recent advances in the bioanalysis of acylcarnitines: Methodologies, challenges, and clinical perspectives.Pharmaceutical science advances · 2026Review
- Altered Acylcarnitine Metabolism in cardiac diseases: From molecular mechanisms to translational potential.International journal of cardiology. Heart & vasculature · 2026Review
- Broad-Coverage Lipidomics Reveals Temporal Lipid Remodeling and Candidate Serum Biomarkers After Acute Spinal Cord Injury in Rats.Biomedicines · 2026Article
- Carnitine dysregulation in diabetic kidney disease: from pathogenic mechanism to precision biomarker.Journal of translational medicine · 2026Review
- Untargeted plasma metabolomics reveals systemic metabolic dysregulation and reatment-associated metabolic modulation following YWKS treatment in sleep disorder patients.Frontiers in pharmacology · 2026Article
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Authors and funding
16 authors.
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Abstract
Approximately 20% of acute myocardial infarction (AMI) patients with multivessel disease experience adverse outcomes after complete revascularization. We aim to investigate the underlying metabolic mechanism of ischemia-reperfusion injury responsible for abnormal hemodynamic stresses in high-risk patients undergoing complete revascularization. Elevated preoperative serum levels of long-chain acylcarnitine (LCAC) 16:1 are associated with an increased risk of poor prognosis following complete revascularization. Multi-omics analyses reveal that reperfusion injury activates fatty acid degradation, and carnitine palmitoyltransferase 1A (CPT1A) is identified as a key regulator of LCACs in the interaction network in porcine models. In the early stages of reperfusion injury in non-culprit lesions, the release and prolonged elevation of circulating LCACs primarily depend on the activation of endothelial CPT1A through hemodynamic injury, which can be reduced using an inhibitor (etomoxir). Excess LCACs enter cardiomyocytes via the organic cation transporter 2, leading to imbalanced mitochondrial quality control and causing cardiomyocyte death.
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