Why the study?
To review advances and discuss potential links between Cullin deneddylation and necroptotic pathways to identify potential therapeutic targets for preventing cardiomyocyte death.
Cullin deneddylation by the COP9 signalosome is essential for cardiomyocyte survival, and its disruption triggers RIPK1-RIPK3-mediated necroptosis and dilated cardiomyopathy.
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Preclinical mouse data identify a survival role for Cullin deneddylation; leaves open whether RIPK1-RIPK3 targeting has therapeutic value in human cardiomyopathy.
Lewno et al. (2021) studied this question.
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