Higher Cardiac Ischemia and Reperfusion Tolerance in Complex III–deficient (Uqcrh-KO) Mice Is Associated with a Shift from Oxidative to Anaerobic Metabolism

Background: The mitochondrial electron transport chain (ETC) is the central building block for oxidative metabolism and ATP production, and thus stalling of electron flux through the ETC commonly compromises cardiac contractile function. Recently, we generated a knockout mouse model of the Uqcrh gene (Uqcrh-KO), which is essential for electron transfer between cytochrome c1 and c of the mitochondrial cytochrome bc1 complex (cIII). Uqcrh-KO mice present with impaired cIII maturation and catalytic function, marked developmental delay, global metabolic abnormalities such as hyperglycemia, and premature death. Here we set out to test how Uqcrh-KO affects cardiac contractile function and substrate use in the unstressed and postischemic heart.