A key mitochondrial protein influences the heart’s ‘fight or flight’ response, a Nature Communications study in mice demonstrates. This may lead to the development of therapies that target this molecule, which could be used to help control excessive heart rate increases.
When stressed, we experience the ‘fight or flight’ response, a suite of physiological changes that includes increased heart rate. However, the molecular mechanisms underpinning this increase in heartbeat are not well defined. Mark Anderson and colleagues now implicate the mitochondrial calcium uniporter (MCU), a protein found in the membranes of tiny, energy-generating cellular organelles called mitochondria, where it helps transport calcium ions into the battery-like structure.
Mice with a faulty version of the protein have normal resting heart rates, but an abnormal response to stress - when the animals are restrained their heart rate does not increase as would be expected. Current drugs designed to dampen excessive heart rates are problematic because they also reduce resting heart rates. Therapies that target the MCU are potentially more beneficial because they have the potential to dampen abnormal increases without affecting resting heart rate.
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