McCaffery Jeanne M, Frasure-Smith Nancy, Dubé Marie-Pierre, Théroux Pierre, Rouleau Guy A, Duan Qingling, Lespérance Francois
Weight Control and Diabetes Research Center, Brown Medical School, Miriam Hospital, Providence, RI, USA.
Psychosom Med. 2006 Mar-Apr;68(2):187-200. doi: 10.1097/01.psy.0000208630.79271.a0.
Although it is well established that depressive symptoms are associated with recurrent cardiac events among cardiac patients and novel cardiac events among participants with no known coronary artery disease (CAD), the nature of this association remains unclear. In this regard, little attention has been paid to the possibility that common genetic vulnerability contributes to both depressive symptoms and CAD. In this paper, we review the existing evidence for common genetic contributions to depression and CAD, primarily using evidence from twin and family studies, followed by a review of two major pathophysiological mechanisms thought to underlie covariation between depressive symptoms and CAD: inflammation and serotonin. We conclude with an overview of select candidate genes within these pathways.
Literature review.
In twin studies, both depression and CAD appear heritable. In the only twin study to consider depression and CAD jointly, the correlation across heritabilities was 0.42, suggesting that nearly 20% of variability in depressive symptoms and CAD was attributable to common genetic factors. In addition, although it is plausible that genetic variation related to inflammation and serotonin may be associated with both depression and CAD, genetic variation related to inflammation has been primary examined in relation to CAD, whereas genetic variation in the serotonin system has been primarily examined in relation to depression.
It appears that the covariation of depressive symptoms and CAD may be attributable, in part, to a common genetic vulnerability. Although several pathways may be involved, genes within the inflammation and serotonin pathways may serve as good candidates for the first steps in identifying genetic variation important for depression, CAD or both.
虽然已有充分证据表明，抑郁症状与心脏病患者的心脏事件复发以及无已知冠状动脉疾病（CAD）参与者的新发心脏事件相关，但这种关联的本质仍不清楚。在这方面，很少有人关注共同的遗传易感性可能导致抑郁症状和CAD这一可能性。在本文中，我们主要利用双胞胎和家族研究的证据，综述了关于抑郁和CAD共同遗传因素的现有证据，随后综述了被认为是抑郁症状和CAD共变基础的两种主要病理生理机制：炎症和血清素。我们最后概述了这些途径中的一些候选基因。
文献综述。
在双胞胎研究中，抑郁和CAD似乎都具有遗传性。在唯一一项同时考虑抑郁和CAD的双胞胎研究中，遗传度之间的相关性为0.42，这表明抑郁症状和CAD近20%的变异性可归因于共同的遗传因素。此外，虽然与炎症和血清素相关的基因变异可能与抑郁和CAD都有关这一点似乎合理，但与炎症相关的基因变异主要是在与CAD相关的研究中进行检测的，而血清素系统的基因变异主要是在与抑郁相关的研究中进行检测的。
抑郁症状和CAD的共变似乎部分可归因于共同的遗传易感性。虽然可能涉及多种途径，但炎症和血清素途径中的基因可能是识别对抑郁、CAD或两者都重要的基因变异的第一步的良好候选基因。
