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Cardiac ischaemia\u2010reperfusion injury (IRI) is in principle a metabolic pathology as it is caused by abruptly halted metabolism during the ischaemic episode and exacerbated by sudden restart of specific metabolic pathways at reperfusion. It should therefore not come as a surprise that therapy directed at metabolic pathways can modulate IRI. Here, we summarize the current knowledge of important metabolic pathways as therapeutic targets to combat cardiac IRI. Activating metabolic pathways such as glycolysis (eg AMPK activators), glucose oxidation (activating pyruvate dehydrogenase complex), ketone oxidation (increasing ketone plasma levels), hexosamine biosynthesis pathway (O\u2010GlcNAcylation; administration of glucosamine\/glutamine) and deacetylation (activating sirtuins 1 or 3; administration of NAD\n                    <jats:sup>+<\/jats:sup>\n                    \u2010boosting compounds) all seem to hold promise to reduce acute IRI. In contrast, some metabolic pathways may offer protection through diminished activity. These pathways comprise the malate\u2010aspartate shuttle (in need of novel specific reversible inhibitors), mitochondrial oxygen consumption, fatty acid oxidation (CD36 inhibitors, malonyl\u2010CoA decarboxylase inhibitors) and mitochondrial succinate metabolism (malonate). Additionally, protecting the cristae structure of the mitochondria during IR, by maintaining the association of hexokinase II or creatine kinase with mitochondria, or inhibiting destabilization of F\n                    <jats:sub>O<\/jats:sub>\n                    F\n                    <jats:sub>1<\/jats:sub>\n                    \u2010ATPase dimers, prevents mitochondrial damage and thereby reduces cardiac IRI. Currently, the most promising and druggable metabolic therapy against cardiac IRI seems to be the singular or combined targeting of glycolysis, O\u2010GlcNAcylation and metabolism of ketones, fatty acids and succinate.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.15180","type":"journal-article","created":{"date-parts":[[2020,5,8]],"date-time":"2020-05-08T18:38:18Z","timestamp":1588963098000},"page":"5937-5954","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":232,"title":["Cardiac metabolism as a driver and therapeutic target of myocardial infarction"],"prefix":"10.1111","volume":"24","author":[{"given":"Coert J.","family":"Zuurbier","sequence":"first","affiliation":[{"name":"Department of Anesthesiology Laboratory of Experimental Intensive Care and Anesthesiology Amsterdam Infection &amp; Immunity Amsterdam Cardiovascular Sciences Amsterdam UMC University of Amsterdam Amsterdam The 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