Necroptosis Signaling Pathways in Stroke: From Mechanisms to Therapies

Title:Necroptosis Signaling Pathways in Stroke: From Mechanisms to Therapies

Volume: 16 Issue: 9

Author(s): Huang Jun-Long, Li Yi, Zhao Bao-Lian, Li Jia-Si, Zhang Ning, Ye Zhou-Heng, Sun Xue-Jun*Liu Wen-Wu*

Affiliation:

• Department of Navy Aviation Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433,China

• Department of Diving and Hyperbaric Medicine, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433,China

Keywords: Programmed cell death, necroptosis, stroke, RIP1, RIP3, MLKL, Nec-1.

Abstract: It has been confirmed that apoptosis, autophagy and necrosis are the three major modes of cell death. For a long time, necrosis is regarded as a deranged or accidental cell demise. In recent years, there is evidence showing that necrotic cell death can be a well regulated and orchestrated event, which is also known as programmed cell death or "necroptosis”. Necroptosis can be triggered by a variety of external stimuli and regulated by a caspase-independent pathway. It plays a key role in the pathogenesis of some diseases including neurological diseases. In the past two decades, a variety of studies have revealed that the necroptosis related pathway is activated in stroke, and plays a crucial role in the pathogenesis of stroke. Moreover, necroptosis may serve as a potential target in the therapy of stroke because genetic or pharmacological inhibition of necroptosis has been shown to be neuroprotective in stroke in vitro and in vivo. In this review, we briefly summarize recent advances in necroptosis, introduce the mechanism and strategies targeting necroptosis in stroke, and finally propose some issues in the treatment of stroke by targeting necroptosis.

Cite this article as:

Jun-Long Huang , Yi Li , Bao-Lian Zhao, Jia-Si Li , Ning Zhang , Zhou-Heng Ye , Xue-Jun Sun *, Wen-Wu Liu *, Necroptosis Signaling Pathways in Stroke: From Mechanisms to Therapies, Current Neuropharmacology 2018; 16 (9) . https://dx.doi.org/10.2174/1570159X16666180416152243