Mitochondrial iron dyshomeostasis and its potential as a therapeutic target for Parkinson's disease.
Exp Neurol
; 372: 114614, 2024 02.
Article
em En
| MEDLINE
| ID: mdl-38007207
ABSTRACT
Abnormal iron accumulation has been implicated in the etiology of Parkinson's disease (PD). Understanding how iron damages dopaminergic neurons in the substantia nigra (SN) of PD is particularly important for developing targeted neurotherapeutic strategies for the disease. However, it is still not fully understood how excess iron contributes to the neurodegeneration of dopaminergic neurons in PD. There has been increased attention on mitochondrial iron dyshomeostasis, iron-induced mitochondrial dysfunction and ferroptosis in PD. Therefore, this review begins with a brief introduction to describe cellular iron metabolism and the dysregulation of iron metabolism in PD. Then we provide an update on how iron is delivered to mitochondria and induces the damage of dopaminergic neurons in PD. In addition, we also summarize new research progress on iron-dependent ferroptosis in PD and mitochondria-localized proteins involved in ferroptosis. This will provide new insight into potential therapeutic strategies targeting mitochondrial iron dysfunction.
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Base de dados:
MEDLINE
Assunto principal:
Doença de Parkinson
Limite:
Humans
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article