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A new insight into an alternative therapeutic approach to restore redox homeostasis and functional mitochondria in neurodegenerative diseases

Title
A new insight into an alternative therapeutic approach to restore redox homeostasis and functional mitochondria in neurodegenerative diseases
Authors
Hyun D.-H.Lee J.
Ewha Authors
현동훈
SCOPUS Author ID
현동훈scopus
Issue Date
2022
Journal Title
Antioxidants
ISSN
2076-3921JCR Link
Citation
Antioxidants vol. 11, no. 1
Keywords
Mitochondrial biogenesisMitochondrial dynamicsMitochondrial dysfunctionNeurodegenerative diseasesNeuroinflammationOxidative stressPlasma membrane redox enzymes
Publisher
MDPI
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Review
Abstract
Neurodegenerative diseases are accompanied by oxidative stress and mitochondrial dys-function, leading to a progressive loss of neuronal cells, formation of protein aggregates, and a decrease in cognitive or motor functions. Mitochondrial dysfunction occurs at the early stage of neurodegenerative diseases. Protein aggregates containing oxidatively damaged biomolecules and other misfolded proteins and neuroinflammation have been identified in animal models and patients with neurodegenerative diseases. A variety of neurodegenerative diseases commonly exhibits decreased activity of antioxidant enzymes, lower amounts of antioxidants, and altered cellular signalling. Although several molecules have been approved clinically, there is no known cure for neurodegenerative diseases, though some drugs are focused on improving mitochondrial function. Mitochondrial dysfunction is caused by oxidative damage and impaired cellular signalling, including that of peroxisome proliferator-activated receptor gamma coactivator 1α. Mitochondrial function can also be modulated by mitochondrial biogenesis and the mitochondrial fusion/fission cycle. Mitochondrial biogenesis is regulated mainly by sirtuin 1, NAD+, AMP-activated protein kinase, mammalian target of rapamycin, and peroxisome proliferator-activated receptor γ. Altered mito-chondrial dynamics, such as increased fission proteins and decreased fusion products, are shown in neurodegenerative diseases. Due to the restrictions of a target-based approach, a phenotype-based approach has been performed to find novel proteins or pathways. Alternatively, plasma membrane redox enzymes improve mitochondrial function without the further production of reactive oxygen species. In addition, inducers of antioxidant response elements can be useful to induce a series of detoxifying enzymes. Thus, redox homeostasis and metabolic regulation can be important therapeutic targets for delaying the progression of neurodegenerative diseases. © 2021 by the authors. Licensee MDPI, Basel, Switzerland.
DOI
10.3390/antiox11010007
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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