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Significance Metabolic dysfunction associated with decreased mitochondrial oxidative capacity is a major underlying cause of heart failure. Our study sheds new light on the potential role of bacteria-derived or endogenous siderophores as direct regulators of cardiomyocyte mitochondrial function. Furthermore, we demonstrate that lipocalin-2, a key feature of the innate immune response, facilitates the transport of siderophore–iron complexes into cells. This mechanism may have important physiological implications because elevated lipocalin-2 levels correlate positively with heart failure in humans, and mice lacking lipocalin-2 are protected from stress-induced mitochondrial dysfunction and heart failure.

Holo-lipocalin-2–derived siderophores increase mitochondrial ROS and impair oxidative phosphorylation in rat cardiomyocytes