Ischaemia‐reperfusion injury (IRI) is associated with programmed cell death that promotes inflammation and organ dysfunction. Necroptosis is mediated by members of receptor interacting protein kinases (RIPK1/3). Inhibition of RIPK1/3 provides… Click to show full abstract
Ischaemia‐reperfusion injury (IRI) is associated with programmed cell death that promotes inflammation and organ dysfunction. Necroptosis is mediated by members of receptor interacting protein kinases (RIPK1/3). Inhibition of RIPK1/3 provides a pro‐survival benefit in kidney IRI. Caspase‐8 initiates apoptosis and contributes to IRI. We studied whether inhibiting both RIPK3 and caspase‐8 would provide an additional benefit in kidney IRI.
               
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