Inflammatory markers in depression
Inflammatory markers in depression
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DOI：
10.1097/yco.0b013e328315a561
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发表时间：
2009-01-01
影响因子：
6.9
通讯作者：
Dinan, Timothy G.
中科院分区：
文献类型：
--
作者：
Dinan, Timothy G.
综述目的提供关于抑郁症和炎症之间联系的文献的重要更新，以及可能的潜在机制和心血管疾病的长期风险。最近的发现当前的文献进一步支持了这样的观点，即重度抑郁症与促炎症反应相关，如 C 反应蛋白和细胞因子（如白细胞介素 6 和肿瘤坏死因子-a）的升高所表明。抗抑郁药抑制炎症反应，而电休克治疗则急剧增加促炎细胞因子水平。大多数（尽管不是全部）研究都支持抑郁、炎症和心血管事件之间的联系。总结抑郁是一种炎症状态，可能会增加心脏病的风险。免疫系统是否是抗抑郁药物开发的适当目标尚未确定。
Purpose of reviewTo provide a critical update of the literature linking depression and inflammation, together with possible underlying mechanisms and longer term risk of cardiovascular disease.Recent findingsThe current literature lends further support to the view that major depression is associated with a proinflammatory response, as indexed by elevation in C-reactive protein and cytokines such as interleukin 6 and tumour necrosis factor-a. Antidepressants suppress the inflammatory response, whereas electroconvulsive therapy acutely increases proinflammatory cytokine levels. Most, though not all, studies support a link between depression, inflammation and cardiovascular events.SummaryDepression is an inflammatory state that may increase the risk of cardiac disease. Whether or not the immune system is an appropriate target for antidepressant development has yet to be established.