{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["6(12)"],"submitter":["Lin R"],"pubmed_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,"],"journal":["Cell reports. Medicine"],"pagination":["102507"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12765950"],"repository":["biostudies-literature"],"pubmed_title":["Targeting long-chain acylcarnitine accumulation to protect cardiac mitochondrial homeostasis after complete revascularization."],"pmcid":["PMC12765950"],"pubmed_authors":["Yin W","Lin R","Qin J","Li F","Gao H","Wang L","Li Y","Tan X","Ren L","Chen W","Wang X","Du J","Wang Y","Yang S","Wang Z"],"additional_accession":[]},"is_claimable":false,"name":"Targeting long-chain acylcarnitine accumulation to protect cardiac mitochondrial homeostasis after complete revascularization.","description":"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,","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-06T11:16:28.569Z","creation":"2026-05-29T03:12:42.379Z"},"accession":"S-EPMC12765950","cross_references":{"pubmed":["41406945"],"doi":["10.1016/j.xcrm.2025.102507"]}}