Electrical power fuels rotary ATP synthase. Mitochondrial calcium signaling and energy metabolism. ATP synthesis by F-type ATP synthase is obligatorily dependent on the transmembrane voltage. MICU1 regulation of mitochondrial Ca(2+) uptake dictates survival and tissue regeneration. MICU1 is an essential gatekeeper for MCU-mediated mitochondrial Ca(2+) uptake that regulates cell survival. The mitochondrial uniporter controls fight or flight heart rate increases. The mitochondrial calcium uniporter selectively matches metabolic output to acute contractile stress in the heart. The mitochondrial calcium uniporter matches energetic supply with cardiac workload during stress and modulates permeability transition. Evolutionary diversity of the mitochondrial calcium uniporter. The mitochondrial calcium uniporter is a highly selective ion channel. Regulation of mitochondrial by cytosolic and work in trabeculae from hypertrophic and normal rat hearts. Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism. Mechanochemotransduction during cardiomyocyte contraction is mediated by localized nitric oxide signaling. Mitochondrial Ca 2+ transport and the role of intramitochondrial Ca 2+ in the regulation of energy metabolism. Role of mitochondrial Ca 2+ in the regulation of cellular energetics. The effects of calcium ions and adenine nucleotides on the activity of pig heart 2-oxoglutarate dehydrogenase complex. Stimulation by calcium ions of pyruvate dehydrogenase phosphate phosphatase. The ADP-ATP translocation in mitochondria, a membrane potential controlled transport. Respiratory enzymes in oxidative phosphorylation. The growing importance of mitochondrial calcium in health and disease. Mitochondrial and nuclear DNA matching shapes metabolism and healthy ageing. Mitochondrial respiratory-chain diseases. Mitochondrial function, biology, and role in disease: a scientific statement from the American Heart Association. Specific metabolic rates of major organs and tissues across adulthood: evaluation by mechanistic model of resting energy expenditure. Respiratory control and the integration of heart high-energy phosphate metabolism by mitochondrial creatine kinase. Activity of the mitochondrial calcium uniporter varies greatly between tissues. These results suggest that, while the conduction of cytosolic Ca 2+ signals through the MCU appears to be tissue dependent, as shown by earlier work 1, the control of ATP synthase by Δ Ψ m appears to be broadly consistent among tissues but is clearly different from that in bacteria.įieni, F., Lee, S. Skeletal muscle MCU Ca 2+ flux, while also having no apparent cytosolic Ca 2+ threshold, is substantially different from the cardiac MCU, yet the ATP synthase voltage dependence in skeletal muscle is identical to that in the heart. Cardiac ATP synthase operates with a different Δ Ψ m threshold for ATP production than bacterial ATP synthase and reveals a concave-upward shape without saturation. Examining the Δ Ψ m dependence of ATP production over the range of −60 mV to −170 mV in detail reveals that cardiac ATP synthase has a voltage dependence that distinguishes it fundamentally from the previous standard, the bacterial ATP synthase. This regulation occurs through matrix Ca 2+-dependent modulation of pyruvate and glutamate dehydrogenase activity and not through any effect of Ca 2+ on ATP synthase or on electron transport chain complexes II, III or IV. We find that the entry of Ca 2+ into the matrix through the mitochondrial calcium uniporter (MCU) in the heart has neither an apparent cytosolic Ca 2+ threshold nor a gating function, and guides ATP production by its influence on the inner mitochondrial membrane (IMM) potential, Δ Ψ m. Here, we investigate the molecular controls of this process in the heart and provide a framework for its Ca 2+-dependent regulation. The regulation of ATP production by mitochondria, crucial for multicellular life, is poorly understood.
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