Driving factors of neuronal ferroptosis

被引:13
作者
Jacquemyn, Julie [1 ,2 ]
Ralhan, Isha [1 ,2 ]
Ioannou, Maria S. [1 ,2 ,3 ,4 ]
机构
[1] Univ Alberta, Dept Physiol, Edmonton, AB T6G 2R3, Canada
[2] Univ Alberta, Grp Mol & Cell Biol Lipids, Edmonton, AB T6G 2R3, Canada
[3] Univ Alberta, Dept Cell Biol, Edmonton, AB T6G 2R3, Canada
[4] Univ Alberta, Neurosci & Mental Hlth Inst, Edmonton, AB T6G 2R3, Canada
基金
加拿大健康研究院;
关键词
AMYLOID PRECURSOR PROTEIN; GLUTATHIONE-PEROXIDASE; 4; OXIDATIVE STRESS; ALPHA-SYNUCLEIN; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; COGNITIVE IMPAIRMENT; LIPID-PEROXIDATION; AMINO-ACIDS; CELL-DEATH;
D O I
10.1016/j.tcb.2024.01.010
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Ferroptosis is an oxidative form of iron-dependent cell death characterized by the accumulation of lipid peroxides on membranes. Iron and lipids containing polyunsaturated fatty acids are essential for this process. Ferroptosis is central to several neurological diseases and underlies the importance of balanced iron and polyunsaturated fatty acid metabolism in the brain, particularly in neurons. Here, we reflect on the potential links between neuronal physiology and the accumulation of iron and peroxidated lipids, the mechanisms neurons use to protect themselves from ferroptosis, and the relationship between pathogenic protein deposition and ferroptosis in neurodegenerative disease. We propose that the unique physiology of neurons makes them especially vulnerable to ferroptosis.
引用
收藏
页码:535 / 546
页数:12
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