transcriptomic differences between ACMs stimulated with a high LCAC C16 concentration and control

About 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 of in high-risk patients undergoing complete revascularization. Elevated preoperative serum levels of long-chain acylcarnitine (LCAC) 16:1 was associated with an increased risk of poor prognosis following complete revascularization. Multi-omics analyses revealed reperfusion injury activates fatty acid degradation and carnitine palmitoyltransferase 1A (CPT1A) was identified as a key regulator of LCACs in the interaction network in the 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 inhibitor (etomoxir). Excess LCACs entered cardiomyocytes via the organic cation transporter 2, leading to imbalanced mitochondrial quality control and causing cardiomyocyte death. Overall design: To determine how LCACs affect mitochondrial dysfunction in cardiomyocytes, we investigated the transcriptomic differences between ACMs stimulated with a high LCAC C16 concentration (150 µM) and control cells by transcriptome sequencing.