Zinc Accumulation Aggravates Cerebral Ischemia/Reperfusion Injury Through Inducing Endoplasmic Reticulum Stress

Zinc is highly enriched in the central nervous system. Numerous evidences suggest that high concentration of zinc acts as a critical mediator of neuronal death in the ischemic brain, however, the possible mechanisms of neurotoxicity of zinc during cerebral ischemia/reperfusion (I/R) remain elusive....

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Veröffentlicht in:	Neurochemical research 2022-05, Vol.47 (5), p.1419-1428
Hauptverfasser:	Zhao, Yongmei, Ding, Mao, Yang, Nan, Huang, Yuyou, Sun, Chengjiao, Shi, Wenjuan
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis Bcl-2 protein Biochemistry Biomedical and Life Sciences Biomedicine Brain Brain Ischemia - metabolism Caspase-12 CCAAT/enhancer-binding protein Cell Biology Cell death Central nervous system Cerebral blood flow Chelation Dementia disorders Endoplasmic reticulum Endoplasmic Reticulum Stress Homology Initiation factor eIF-2α Injuries Intracellular Ischemia Lymphocytes B Lymphoma Male Mortality Neurochemistry Neurology Neurosciences Neurotoxicity Occlusion Original Paper Proteins Rats Rats, Sprague-Dawley Reperfusion Reperfusion Injury - metabolism Staining Stress Vascular dementia Zinc
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