The possible roles of necroptosis during cerebral ischemia and ischemia / reperfusion injury.

The possible roles of necroptosis during cerebral ischemia and ischemia / reperfusion injury. Arch Biochem Biophys. 2020 Oct 14;695:108629 Authors: Liao S, Apaijai N, Chattipakorn N, Chattipakorn SC Abstract Cell death is a process consequential to cerebral ischemia and cerebral ischemia/reperfusion (I/R) injury. Recent evidence suggest that necroptosis has been involved in the pathogenesis of ischemic brain injury. The mechanism of necroptosis is initiated by an activation of inflammatory receptors including tumor necrosis factor, toll like receptor, and fas ligands. The signals activate the receptor-interacting protein kinase (RIPK) 1, 3, and a mixed-lineage kinase domain-like pseudokinase (MLKL) to instigate necroptosis. RIPK1 inhibitor, necrostatin-1, was developed, and dramatically reduced brain injury following cerebral ischemia in mice. Consequently, necroptosis could be a novel therapeutic target for stroke, which aims to reduce long-term adverse outcomes after cerebral ischemia. Several studies have been conducted to test the roles of necroptosis on cerebral ischemia and cerebral I/R injury, and the efficacy of necrostatin-1 has been tested in those models. Evidence regarding the roles of necroptosis and the effects of necrostatin-1, from in vitro and in vivo studies, has been summarized and discussed. In addition, other therapeutic managements, involving in necroptosis, are also included in this review. We believe that the ...
Source: Archives of Biochemistry and Biophysics - Category: Biochemistry Authors: Tags: Arch Biochem Biophys Source Type: research