Necroptosis in Acute Kidney Injury

Acute kidney injury (AKI) is a common clinical entity associated with high morbidity and mortality. Tubular epithelial cell death plays a key role in the development of AKI. Although apoptosis has been the focus of the studies on kidney injury and drug discovery for many years, recent studies have identified signaling pathways and regulatory mechanisms for programmed necrosis or necroptosis. It is now clear that receptor-interacting kinase 1 (RIP1), RIP3 and its substrate, the pseudokinase mixed lineage kinase domain-like protein (MLKL) are the core components of necroptosis. Increasing evidence from pharmacological and genetic studies shows that necroptosis plays critical roles in progression of AKI in several mouse models. In this review, we aim to briefly summarize the mechanisms and functions of necroptosis in AKI.