ArticleCardiovascular research2021
Mechanism of succinate efflux upon reperfusion of the ischaemic heart.
Article in Cardiovascular research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 105 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
- Resistance to atrial fibrillation domestication and mitochondrial dysfunction in sheep: a potential key role of the TCA cycle and mitochondrial redox state.Redox biology · 2026Article
- A positively selected microRNA controls a reversible aging program in striated muscle.bioRxiv : the preprint server for biology · 2026Article
- Review
- Multiple organ dysfunction syndrome: molecular mechanisms and therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Succinate and lactate produced as conserved biomarkers through chronic and transient substrate-level phosphorylation: from microorganisms to cancer.Journal of bioenergetics and biomembranes · 2026Review
- CK2α Deficiency Drives Myocardial Fibrosis via Desmin-Induced Mitochondrial Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Mechanisms Involved in Pathological Succinate-Mediated Signaling.International journal of molecular sciences · 2026Review
- Mitochondrial succinate transport is required for cardiac ischaemia/reperfusion injury.Cardiovascular research · 2026Article
- The role and therapeutic potential of succinate and succinylation in cardiovascular diseases.Clinical epigenetics · 2026Review
- Mitochondrial responses to anoxia-reoxygenation exposure in crucian carp (Carassius carassius).The Journal of experimental biology · 2026Article
- Targeting immunometabolic pathways with AZD1656 alleviates inflammation and metabolic dysfunction in type 2 diabetic cardiomyopathy.Nature cardiovascular research · 2026Article
- Plasma and pericardial fluid metabolomic signatures of patients with ischemic heart disease.Communications medicine · 2026Article
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.Frontiers in immunology · 2026Review
- Methylmalonate accumulation contributes to myocardial vulnerability post-reperfusion: a novel therapeutic target and prognostic biomarker.BMC medicine · 2025Article
- Emerging roles of the metabolite succinate in bone-related diseases.Journal of Zhejiang University. Science. B · 2025Review
- Succinate-GPR91 signaling promotes cardiomyocyte metabolic reprogramming and NADCardiovascular diabetology · 2025Article
- Simultaneous and sensitive quantification of protein and low molecular weight persulfides, polysulfides and HNature communications · 2025Article
- Rapid mitochondrial repolarization upon reperfusion after cardiac ischemia.Nature cardiovascular research · 2025Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
Abstract
aimsSuccinate accumulates several-fold in the ischaemic heart and is then rapidly oxidized upon reperfusion, contributing to reactive oxygen species production by mitochondria. In addition, a significant amount of the accumulated succinate is released from the heart into the circulation at reperfusion, potentially activating the G-protein-coupled succinate receptor (SUCNR1). However, the factors that determine the proportion of succinate oxidation or release, and the mechanism of this release, are not known. METHODS AND
resultsTo address these questions, we assessed the fate of accumulated succinate upon reperfusion of anoxic cardiomyocytes, and of the ischaemic heart both ex vivo and in vivo. The release of accumulated succinate was selective and was enhanced by acidification of the intracellular milieu. Furthermore, pharmacological inhibition, or haploinsufficiency of the monocarboxylate transporter 1 (MCT1) significantly decreased succinate efflux from the reperfused heart.
conclusionSuccinate release upon reperfusion of the ischaemic heart is mediated by MCT1 and is facilitated by the acidification of the myocardium during ischaemia. These findings will allow the signalling interaction between succinate released from reperfused ischaemic myocardium and SUCNR1 to be explored.
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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.