Psychological Stress and Mitochondria: A Systematic Review

被引:170
|
作者
Picard, Martin [1 ,2 ,3 ]
McEwen, Bruce S. [4 ]
机构
[1] Columbia Univ, Dept Psychiat, Div Behav Med, New York, NY USA
[2] Columbia Univ, Dept Neurol, H Houston Merritt Ctr, Columbia Translat Neurosci Initiat, New York, NY USA
[3] Columbia Univ, Columbia Aging Ctr, New York, NY USA
[4] Rockefeller Univ, Neuroendocrinol Lab, 1230 York Ave, New York, NY 10021 USA
基金
美国国家卫生研究院;
关键词
psychological; psychosocial stress; mitochondria; systematic review; psychosomatic medicine; psychoneuroendocrinology; INDUCED COGNITIVE IMPAIRMENT; OXIDATIVE STRESS; SKELETAL-MUSCLE; PSYCHOSOCIAL STRESS; RESPIRATORY-CHAIN; TRAIT ANXIETY; CYTOCHROME-C; MOUSE MODEL; DNA; BRAIN;
D O I
10.1097/PSY.0000000000000545
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
Objective Mitochondria are multifunctional life-sustaining organelles that represent a potential intersection point between psychosocial experiences and biological stress responses. This article provides a systematic review of the effects of psychological stress on mitochondrial structure and function. Methods A systematic review of the literature investigating the effects of psychological stress on mitochondrial function was conducted. The review focused on experimentally controlled studies allowing us to draw causal inference about the effect of induced psychological stress on mitochondria. Results A total of 23 studies met the inclusion criteria. All studies involved male laboratory animals, and most demonstrated that acute and chronic stressors influenced specific facets of mitochondrial function, particularly within the brain. Nineteen studies showed significant adverse effects of psychological stress on mitochondria and four found increases in function or size after stress. In humans, only six observational studies were available, none with experimental designs, and most only measured biological markers that do not directly reflect mitochondrial function, such as mitochondrial DNA copy number. Conclusons Overall, evidence supports the notion that acute and chronic stressors influence various aspects of mitochondrial biology, and that chronic stress exposure can lead to molecular and functional recalibrations among mitochondria. Limitations of current animal and human studies are discussed. Maladaptive mitochondrial changes that characterize this subcellular state of stress are termed mitochondrial allostatic load. Prospective studies with sensitive measures of specific mitochondrial outcomes will be needed to establish the link between psychosocial stressors, emotional states, the resulting neuroendocrine and immune processes, and mitochondrial energetics relevant to mind-body research in humans.
引用
收藏
页码:141 / 153
页数:13
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