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Mitochondrial Metabolism in Major Neurological Diseases
被引:52
作者:
Zhou, Zhengqiu
[1
]
Austin, Grant L.
[1
]
Young, Lyndsay E. A.
[1
]
Johnson, Lance A.
[2
]
Sun, Ramon
[1
]
机构:
[1] Univ Kentucky, Mol & Cellular Biochem Dept, Lexington, KY 40536 USA
[2] Univ Kentucky, Dept Physiol, Lexington, KY 40536 USA
来源:
关键词:
metabolism;
mitochondria;
Alzheimer's disease;
epilepsy;
traumatic brain injury;
TRAUMATIC BRAIN-INJURY;
CYTOCHROME-C-OXIDASE;
POSITRON-EMISSION-TOMOGRAPHY;
COMPLEX-I DEFICIENCY;
PYRUVATE-DEHYDROGENASE COMPLEX;
DNA DEPLETION SYNDROME;
FATTY-ACID OXIDATION;
ALZHEIMERS-DISEASE;
APOLIPOPROTEIN-E;
ENERGY-METABOLISM;
D O I:
10.3390/cells7120229
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Mitochondria are bilayer sub-cellular organelles that are an integral part of normal cellular physiology. They are responsible for producing the majority of a cell's ATP, thus supplying energy for a variety of key cellular processes, especially in the brain. Although energy production is a key aspect of mitochondrial metabolism, its role extends far beyond energy production to cell signaling and epigenetic regulation-functions that contribute to cellular proliferation, differentiation, apoptosis, migration, and autophagy. Recent research on neurological disorders suggest a major metabolic component in disease pathophysiology, and mitochondria have been shown to be in the center of metabolic dysregulation and possibly disease manifestation. This review will discuss the basic functions of mitochondria and how alterations in mitochondrial activity lead to neurological disease progression.
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页数:25
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