Ethanol-activated CaMKII signaling induces neuronal apoptosis through Drp1-mediated excessive mitochondrial fission and JNK1-dependent NLRP3 inflammasome activation

Ethanol-activated CaMKII signaling induces neuronal apoptosis through Drp1-mediated excessive mitochondrial fission and JNK1-dependent NLRP3 inflammasome activation

Abstract Background Neurodegeneration is a representative phenotype of patients with chronic alcoholism. Ethanol-induced calcium overload causes NOD-like receptor protein 3 (NLRP3) inflammasome formation and an imbalance in mitochondrial dynamics, closely associated with the pathogenesis of neurodeg...

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Bibliographic Details
Main Authors: Jae Ryong Lim, Hyun Jik Lee, Young Hyun Jung, Jun Sung Kim, Chang Woo Chae, Seo Yihl Kim, Ho Jae Han
Format: Article
Language:English
Published: BMC 2020-08-01
Series:Cell Communication and Signaling
Subjects:
Ethanol
NMDA receptor
NLRP3 inflammasome
CaMKII
JNK1
Drp1
Online Access:http://link.springer.com/article/10.1186/s12964-020-00572-3

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http://link.springer.com/article/10.1186/s12964-020-00572-3

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