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Loss of receptor interacting protein kinases 3 and caspase‐8 augments intrinsic apoptosis in tubular epithelial cell and promote kidney ischaemia‐reperfusion injury

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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.

Keywords: receptor interacting; protein kinases; ischaemia reperfusion; reperfusion injury; interacting protein; kidney

Journal Title: Nephrology
Year Published: 2019

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