ArticleJournal of the American Heart Association2018
Metabolomic Profiling in Acute ST-Segment-Elevation Myocardial Infarction Identifies Succinate as an Early Marker of Human Ischemia-Reperfusion Injury.
Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 87 citations in OpenAlex.
- Spontaneous reperfusion enhances succinate concentration in peripheral blood from stemi patients but its levels does not correlate with myocardial infarct size or area at risk.Scientific reports · 2023Trial
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- ATP5A1 succinylation as a key driver for the transition of myocardial ischemia to development of heart failure.Basic research in cardiology · 2026Article
- Article
- Review
- The metabolic consequences of evoked spreading depolarization in brain slices.Scientific reports · 2026Article
- Dimethyl malonate suppresses succinate dehydrogenase to alleviate ischemia/reperfusion-induced acute lung injury.Frontiers in pharmacology · 2026Article
- Femoral arteriovenous concentration differences reveal metabolomic shifts in peripheral artery disease (PAD): A case-control study.Vascular medicine (London, England) · 2025Article
- Emerging therapy strategies for energy metabolism in acute myocardial infarction.Journal of translational medicine · 2025Review
- Type 2 diabetes worsens the outcome of ischemia/reperfusion in female STEMI patients and female db/db mice with HFpEF cardiometabolic phenotype.Cardiovascular diabetology · 2025Article
- Review
- Injured Myocardium-Targeted Theranostic Nanoplatform for Multi-Dimensional Immune-Inflammation Regulation in Acute Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting Mitochondria for Cancer Treatment.Pharmaceutics · 2024Review
- Residual Complex I activity and amphidirectional Complex II operation support glutamate catabolism through mtSLP in anoxia.Scientific reports · 2024Article
- Phenomic Imaging.Phenomics (Cham, Switzerland) · 2023Review
- Multinomial machine learning identifies independent biomarkers by integrated metabolic analysis of acute coronary syndrome.Scientific reports · 2023Article
- Health position paper and redox perspectives on reactive oxygen species as signals and targets of cardioprotection.Redox biology · 2023Review
- Preventing mitochondrial reverse electron transport as a strategy for cardioprotection.Basic research in cardiology · 2023Review
- Extracellular Succinate: A Physiological Messenger and a Pathological Trigger.International journal of molecular sciences · 2023Review
- Progress in the Metabolomics of Acute Coronary Syndrome.Reviews in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundIschemia-reperfusion injury following ST-segment-elevation myocardial infarction (STEMI) is a leading determinant of clinical outcome. In experimental models of myocardial ischemia, succinate accumulation leading to mitochondrial dysfunction is a major cause of ischemia-reperfusion injury; however, the potential importance and specificity of myocardial succinate accumulation in human STEMI is unknown. We sought to identify the metabolites released from the heart in patients undergoing primary percutaneous coronary intervention for emergency treatment of STEMI. METHODS AND
resultsBlood samples were obtained from the coronary artery, coronary sinus, and peripheral vein in patients undergoing primary percutaneous coronary intervention for acute STEMI and in control patients undergoing nonemergency coronary angiography or percutaneous coronary intervention for stable angina or non-STEMI. Plasma metabolites were analyzed by targeted liquid chromatography and mass spectrometry. Metabolite levels for coronary artery, coronary sinus, and peripheral vein were compared to derive cardiac and systemic release ratios. In STEMI patients, cardiac magnetic resonance imaging was performed 2 days and 6 months after primary percutaneous coronary intervention to quantify acute myocardial edema and final infarct size, respectively. In total, 115 patients undergoing acute STEMI and 26 control patients were included. Succinate was the only metabolite significantly increased in coronary sinus blood compared with venous blood in STEMI patients, indicating cardiac release of succinate. STEMI patients had higher succinate concentrations in arterial, coronary sinus, and peripheral venous blood than patients with non-STEMI or stable angina. Furthermore, cardiac succinate release in STEMI correlated with the extent of acute myocardial injury, quantified by cardiac magnetic resonance imaging.
conclusionSuccinate release by the myocardium correlates with the extent of ischemia.
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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.