The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease

Behavioural Neurology
Yang XuZhaohu Chu

Abstract

Necroptosis is the best-described form of regulated necrosis at present, which is widely recognized as a component of caspase-independent cell death mediated by the concerted action of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3). Mixed-lineage kinase domain-like (MLKL) was phosphorylated by RIPK3 at the threonine 357 and serine 358 residues and then formed tetramers and translocated onto the plasma membrane, which destabilizes plasma membrane integrity leading to cell swelling and membrane rupture. Necroptosis is downstream of the tumor necrosis factor (TNF) receptor family, and also interaction with NOD-like receptor pyrin 3 (NLRP3) induced inflammasome activation. Multiple inhibitors of RIPK1 and MLKL have been developed to block the cascade of signal pathways for procedural necrosis and represent potential leads for drug development. In this review, we highlight recent progress in the study of roles for necroptosis in cerebral ischemic disease and discuss how these modifications delicately control necroptosis.

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Citations

Jun 6, 2019·Journal of Neurochemistry·Enrique Font-BelmonteArsenio Fernández-López
Jun 13, 2019·The Journal of Experimental Medicine·David E Place, Thirumala-Devi Kanneganti
Dec 11, 2019·Cell Biology and Toxicology·J Grace Nirmala, Manu Lopus
Dec 16, 2019·Biochemical and Biophysical Research Communications·Xiaoxue YuTao Shen
Oct 17, 2020·Journal of Molecular Cell Biology·Lu LiXiawei Wei
Jul 28, 2021·RNA Biology·Lei XuYi Zhang

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Methods Mentioned

BETA
gene knockout
GTPase
nuclear translocation

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