New findings indicate a role for mitochondrial dynamics in the pathogenesis of cardiorenal syndrome. Sumida et al. found evidence of mitochondrial fragmentation in the hearts of mice 24 h after renal ischaemia–reperfusion injury (IRI). After 72 h, mice had cardiomyocyte apoptosis and cardiac dysfunction. Levels of Drp1, a regulator of mitochondrial fission, were upregulated in the mitochondrial fraction of the heart and administration of a Drp1 inhibitor before IRI decreased mitochondrial fragmentation and ameliorated cardiac dysfunction.