From stress to inflammation and major depressive disorder: a social signal transduction theory of depression.
From stress to inflammation and major depressive disorder: a social signal transduction theory of depression.
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DOI：
10.1037/a0035302
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发表时间：
2014-05
影响因子：
22.4
通讯作者：
Irwin MR
中科院分区：
文献类型：
--
作者：
Slavich GM;Irwin MR
重大生活压力源，尤其是涉及人际压力和社会排斥的压力源，是抑郁症最强的近端风险因素之一。在这篇综述中，我们提出了一个具有生物学合理性的多层次理论，该理论描述了将社会环境压力经历与驱动抑郁症发病机制的内部生物学过程联系起来的神经、生理、分子和基因组机制。抑郁症的这种社会信号转导理论的核心假设是，社会威胁和逆境经历会上调参与炎症的免疫系统成分。这种反应的关键介质，即促炎细胞因子，反过来又能引起行为的深刻变化，包括引发抑郁症状，如悲伤情绪、快感缺失、疲劳、精神运动迟缓以及社交行为退缩。这种对逆境高度保守的生物学反应在实际身体受到威胁或受伤时对生存至关重要。然而，这种反应也可由现代社会的、象征性的或想象中的威胁所激活，导致一种日益促炎的表型，这可能是驱动抑郁症发病和复发的一个关键现象，也是抑郁症与包括哮喘、类风湿性关节炎、慢性疼痛、代谢综合征、心血管疾病、肥胖和神经退行性变在内的几种躯体疾病状况重叠的原因。因此，该理论的见解可能会阐明几个重要问题，包括抑郁症是如何发展的、为什么它经常复发、为什么它能被早期生活压力强烈预测以及为什么它经常与焦虑症状以及某些躯体疾病状况同时发生。这项工作还可能为通过针对炎症预防和治疗抑郁症提供新的机会。
Major life stressors, especially those involving interpersonal stress and social rejection, are among the strongest proximal risk factors for depression. In this review, we propose a biologically plausible, multilevel theory that describes neural, physiologic, molecular, and genomic mechanisms that link experiences of social-environmental stress with internal biological processes that drive depression pathogenesis. Central to this social signal transduction theory of depression is the hypothesis that experiences of social threat and adversity up-regulate components of the immune system involved in inflammation. The key mediators of this response, called proinflammatory cytokines, can in turn elicit profound changes in behavior, which include the initiation of depressive symptoms such as sad mood, anhedonia, fatigue, psychomotor retardation, and social-behavioral withdrawal. This highly conserved biological response to adversity is critical for survival during times of actual physical threat or injury. However, this response can also be activated by modern-day social, symbolic, or imagined threats, leading to an increasingly proinflammatory phenotype that may be a key phenomenon driving depression pathogenesis and recurrence, as well as the overlap of depression with several somatic conditions including asthma, rheumatoid arthritis, chronic pain, metabolic syndrome, cardiovascular disease, obesity, and neurodegeneration. Insights from this theory may thus shed light on several important questions including how depression develops, why it frequently recurs, why it is strongly predicted by early life stress, and why it often co-occurs with symptoms of anxiety and with certain physical disease conditions. This work may also suggest new opportunities for preventing and treating depression by targeting inflammation.
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影响因子：
10.6
作者：
Antoni, Michael H.;Lutgendorf, Susan K.;Blomberg, Bonnie;Carver, Charles S.;Lechner, Suzanne;Diaz, Alain;Stagl, Jamie;Arevalo, Jesusa M. G.;Cole, Steven W.
通讯作者：
Cole, Steven W.
DOI：
10.1126/science.1179050
发表时间：
2009-10-09
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Amit I;Garber M;Chevrier N;Leite AP;Donner Y;Eisenhaure T;Guttman M;Grenier JK;Li W;Zuk O;Schubert LA;Birditt B;Shay T;Goren A;Zhang X;Smith Z;Deering R;McDonald RC;Cabili M;Bernstein BE;Rinn JL;Meissner A;Root DE;Hacohen N;Regev A
通讯作者：
Regev A
影响因子：
3.7
作者：
Anacker, Christoph;Zunszain, Patricia A.;Carvalho, Livia A.;Pariante, Carmine M.
通讯作者：
Pariante, Carmine M.
影响因子：
3.3
作者：
Bair, MJ;Robinson, RL;Kroenke, K
通讯作者：
Kroenke, K
影响因子：
3.3
作者：
Backonja, Miroslav Misha;Coe, Christopher L.;Schell, Kathleen
通讯作者：
Schell, Kathleen