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Mitochondrial ROS signals prevent excessive immune response

Reactive oxygen species (ROS) were long considered unwanted and dangerous by-products of mitochondrial metabolism, specifically oxidative phosphorylation. More recently, evidence has indicated that mitochondrial ROS are also essential signalling molecules that unexpectedly promote longevity, through a mechanism termed mitohormesis. In this issue, Timblin et al. expand this concept to immunity, specifically macrophage function, by demonstrating that mitochondrial ROS are required to prevent an excessive immune response.

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Fig. 1: Mitohormesis limits an excessive immune response.


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Correspondence to Michael Ristow.

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Zarse, K., Ristow, M. Mitochondrial ROS signals prevent excessive immune response. Nat Metab 3, 588–589 (2021).

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