TY - JOUR
T1 - Necroptosis and Neuroinflammation in Retinal Degeneration
AU - Tao, Yan
AU - Murakami, Yusuke
AU - Vavvas, Demetrios G.
AU - Sonoda, Koh Hei
N1 - Funding Information:
This work was supported by Grants-in-Aid for Scientific Research, #JP19K09952 and #JP22H03242 (to YM), a Uehara Memorial Foundation grant (to YM), a Charitable Trust Fund for Ophthalmic Research in Commemoration of Santen Pharmaceutical's Founder grant (to YM), and a Bayer Retina Award (to YM).
Publisher Copyright:
Copyright © 2022 Tao, Murakami, Vavvas and Sonoda.
PY - 2022/6/29
Y1 - 2022/6/29
N2 - Necroptosis mediates the chronic inflammatory phenotype in neurodegeneration. Receptor-interacting protein kinase (RIPK) plays a pivotal role in the induction of necroptosis in various cell types, including microglia, and it is implicated in diverse neurodegenerative diseases in the central nervous system and the retina. Targeting RIPK has been proven beneficial for alleviating both neuroinflammation and degeneration in basic/preclinical studies. In this review, we discuss the role of necroptosis in retinal degeneration, including (1) the molecular pathways involving RIPK, (2) RIPK-dependent microglial activation and necroptosis, and (3) the interactions between necroptosis and retinal neuroinflammation/degeneration. This review will contribute to a renewed focus on neuroinflammation induced by necroptosis and to the development of anti-RIPK drugs against retinal degeneration.
AB - Necroptosis mediates the chronic inflammatory phenotype in neurodegeneration. Receptor-interacting protein kinase (RIPK) plays a pivotal role in the induction of necroptosis in various cell types, including microglia, and it is implicated in diverse neurodegenerative diseases in the central nervous system and the retina. Targeting RIPK has been proven beneficial for alleviating both neuroinflammation and degeneration in basic/preclinical studies. In this review, we discuss the role of necroptosis in retinal degeneration, including (1) the molecular pathways involving RIPK, (2) RIPK-dependent microglial activation and necroptosis, and (3) the interactions between necroptosis and retinal neuroinflammation/degeneration. This review will contribute to a renewed focus on neuroinflammation induced by necroptosis and to the development of anti-RIPK drugs against retinal degeneration.
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U2 - 10.3389/fnins.2022.911430
DO - 10.3389/fnins.2022.911430
M3 - Review article
AN - SCOPUS:85134149534
VL - 16
JO - Frontiers in Neuroscience
JF - Frontiers in Neuroscience
SN - 1662-4548
M1 - 911430
ER -