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Mood Disorders, Accelerated Aging, and Inflammation: Is the Link Hidden in Telomeres?

机译:情绪障碍,加速衰老和炎症:端粒中是否隐藏链接?

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Mood disorders are associated with an increased risk of aging-related diseases, which greatly contribute to the excess morbidity and mortality observed in affected individuals. Clinical and molecular findings also suggest that mood disorders might be characterized by a permanent state of low-grade inflammation. At the cellular level, aging translates into telomeres shortening. Intriguingly, inflammation and telomere shortening show a bidirectional association: a pro-inflammatory state seems to contribute to aging and telomere dysfunction, and telomere attrition is able to induce low-grade inflammation. Several independent studies have reported shorter telomere length and increased levels of circulating inflammatory cytokines in mood disorders, suggesting a complex interplay between altered inflammatory–immune responses and telomere dynamics in the etiopathogenesis of these disorders. In this review, we critically discuss studies investigating the role of telomere attrition and inflammation in the pathogenesis and course of mood disorders, and in pharmacological treatments with psychotropic medications.
机译:情绪障碍会增加与衰老相关的疾病的风险,这极大地增加了患病个体的发病率和死亡率。临床和分子研究结果还表明,情绪障碍的特征可能是永久性的低度炎症状态。在细胞水平上,衰老转化为端粒缩短。有趣的是,炎症和端粒缩短显示出双向关联:促炎状态似乎促成衰老和端粒功能障碍,端粒损耗能够诱发轻度炎症。几项独立研究报道,情绪障碍中端粒的长度较短,循环炎症细胞因子水平升高,表明这些疾病的病因发病机制中炎症免疫反应的改变与端粒动力学之间存在复杂的相互作用。在这篇综述中,我们严格地讨论了研究端粒磨损和炎症在情绪障碍的发病机理和过程中以及在用精神药物进行药理治疗中的作用的研究。

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