Mitochondrial Dysfunction in Neurodegenerative Diseases and Cancer

被引：186

作者：

de Moura, Michelle Barbi ^{[1
]}

dos Santos, Lucas Santana ^{[1
]}

Van Houten, Bennett ^{[1
]}

机构：

[1] Univ Pittsburgh, Sch Med, Inst Canc, Dept Pharmacol & Chem Biol, Pittsburgh, PA USA

来源：

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS | 2010年 / 51卷 / 05期

关键词：

mitochondria; neurodegenerative disease; cancer; ROS; ATP-CONSUMING PROCESSES; TRANSCRIPTION FACTOR-A; TUMOR-SUPPRESSOR GENE; HUNTINGTONS-DISEASE; PARKINSONS-DISEASE; ALZHEIMERS-DISEASE; DNA DAMAGE; OXIDATIVE STRESS; CELL-DEATH; C-MYC;

D O I：

10.1002/em.20575

中图分类号：

X [环境科学、安全科学];

学科分类号：

08 ; 0830 ;

摘要：

Mitochondria are important integrators of cellular function and therefore affect the homeostatic balance of the cell. Besides their important role in producing adenosine triphosphate through oxidative phosphorylation, mitochondria are involved in the control of cytosolic calcium concentration, metabolism of key cellular intermediates, and Fe/S cluster biogenesis and contributed to programmed cell death. Mitochondria are also one of the major cellular producers of reactive oxygen species (ROS). Several human pathologies, including neurodegenerative diseases and cancer, are associated with mitochondrial dysfunction and increased ROS damage. This article reviews how dysfunctional mitochondria contribute to Alzheimer's disease, Parkinson's disease, Huntington's disease, and several human cancers. Environ. Mol. Mutagen. 51:391-405, 2010. (C) 2010 Wiley-Liss, Inc.

引用

页码：391 / 405

页数：15

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