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Prostanoids put a brake on necroptosis in IBD

A form of programmed cell death, necroptosis, in intestinal epithelial cells initiates mucosal inflammation. A study now finds that prostanoid EP4 receptor signalling interferes with RIPK1–RIPK3-dependent MLKL activation, thereby inhibiting necroptosis and accelerating resolution of inflammation.

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Fig. 1: EP4 agonism blocks epithelial necroptosis and thereby promotes mucosal restitution.


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Correspondence to Arthur Kaser.

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Kaneider, N.C., Kaser, A. Prostanoids put a brake on necroptosis in IBD. Nat Cell Biol 23, 680–681 (2021).

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