期刊
BRITISH JOURNAL OF PHARMACOLOGY
卷 171, 期 8, 页码 2159-2173出版社
WILEY
DOI: 10.1111/bph.12513
关键词
mitochondria; biometal homeostasis; neurodegeneration; stroke; Cu(atsm); Mn porphyrins; curcumin; deferiprone
资金
- ARC Future Fellowship
- NHMRC Biomedical Fellowship
Transition metals are critical for enzyme function and protein folding, but in excess can mediate neurotoxic oxidative processes. As mitochondria are particularly vulnerable to oxidative damage due to radicals generated during ATP production, mitochondrial biometal homeostasis must therefore be tightly controlled to safely harness the redox potential of metal enzyme cofactors. Dysregulation of metal functions is evident in numerous neurological disorders including Alzheimer's disease, stroke, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis and Friedrich's ataxia. This review describes the mitochondrial metal defects in these disorders and highlights novel metal-based therapeutic approaches that target mitochondrial metal homeostasis in neurological disorders. Linked ArticlesThis article is part of a themed issue on Mitochondrial Pharmacology: Energy, Injury & Beyond. To view the other articles in this issue visit
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