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