From the Department of Psychiatry, Division of Behavioral Medicine (Picard), Department of Neurology, The H. Houston Merritt Center, Columbia Translational Neuroscience Initiative (Picard), and Columbia Aging Center (Picard), Columbia University; and Laboratory for Neuroendocrinology (McEwen), The Rockefeller University, New York, New York.
Psychosom Med. 2018 Feb/Mar;80(2):126-140. doi: 10.1097/PSY.0000000000000544.
The integration of biological, psychological, and social factors in medicine has benefited from increasingly precise stress response biomarkers. Mitochondria, a subcellular organelle with its own genome, produce the energy required for life and generate signals that enable stress adaptation. An emerging concept proposes that mitochondria sense, integrate, and transduce psychosocial and behavioral factors into cellular and molecular modifications. Mitochondrial signaling might in turn contribute to the biological embedding of psychological states.
A narrative literature review was conducted to evaluate evidence supporting this model implicating mitochondria in the stress response, and its implementation in behavioral and psychosomatic medicine.
Chronically, psychological stress induces metabolic and neuroendocrine mediators that cause structural and functional recalibrations of mitochondria, which constitutes mitochondrial allostatic load. Clinically, primary mitochondrial defects affect the brain, the endocrine system, and the immune systems that play a role in psychosomatic processes, suggesting a shared underlying mechanistic basis. Mitochondrial function and dysfunction also contribute to systemic physiological regulation through the release of mitokines and other metabolites. At the cellular level, mitochondrial signaling influences gene expression and epigenetic modifications, and modulates the rate of cellular aging.
This evidence suggests that mitochondrial allostatic load represents a potential subcellular mechanism for transducing psychosocial experiences and the resulting emotional responses-both adverse and positive-into clinically meaningful biological and physiological changes. The associated article in this issue of Psychosomatic Medicine presents a systematic review of the effects of psychological stress on mitochondria. Integrating mitochondria into biobehavioral and psychosomatic research opens new possibilities to investigate how psychosocial factors influence human health and well-being across the life-span.
生物学、心理学和社会因素的整合在医学中受益于越来越精确的应激反应生物标志物。线粒体是具有自身基因组的细胞器，产生生命所需的能量，并产生使压力适应的信号。一个新兴的概念提出，线粒体感知、整合和转导心理社会和行为因素，转化为细胞和分子的修饰。线粒体信号可能反过来有助于心理状态的生物学嵌入。
进行了叙述性文献综述，以评估支持这一模型的证据，该模型暗示线粒体参与应激反应，以及其在行为和身心医学中的实施。
长期以来，心理压力会引发代谢和神经内分泌介质，导致线粒体的结构和功能重新校准，这构成了线粒体适应负荷。临床上，原发性线粒体缺陷会影响大脑、内分泌系统和免疫系统，这些系统在身心过程中发挥作用，表明存在共同的潜在机制基础。线粒体功能和功能障碍也通过释放线粒体因子和其他代谢物对全身生理调节做出贡献。在细胞水平上，线粒体信号影响基因表达和表观遗传修饰，并调节细胞衰老的速度。
这一证据表明，线粒体适应负荷代表了一种潜在的亚细胞机制，用于将心理社会体验和由此产生的情绪反应（包括负面和正面）转化为具有临床意义的生物学和生理学变化。本期《身心医学》杂志上的相关文章对心理压力对线粒体的影响进行了系统综述。将线粒体纳入生物行为学和身心研究为研究心理社会因素如何影响人类健康和福祉提供了新的可能性，跨越整个生命周期。
