Wolf Erika J, Morrison Filomene G
National Center for PTSD, VA Boston Healthcare System, (116B-2), 150 South Huntington Ave, Boston, MA, 02130, USA.
Department of Psychiatry, Boston University School of Medicine, Boston, MA, USA.
Curr Psychiatry Rep. 2017 Aug 29;19(10):75. doi: 10.1007/s11920-017-0823-5.
The aim of this paper is to review the recent literature on traumatic stress-related accelerated aging, including a focus on cellular mechanisms and biomarkers of cellular aging and on the clinical manifestations of accelerated biological aging.
Multiple lines of research converge to suggest that PTSD is associated with accelerated aging in the epigenome, and the immune and inflammation systems, and this may be reflected in premature onset of cardiometabolic and cardiovascular disease. The current state of research paves the way for future work focused on identifying the peripheral and central biological mechanisms linking traumatic stress to accelerated biological aging and medical morbidity, with an emphasis on processes involved in inflammation, immune functioning, oxidative stress, autonomic arousal, and stress response. Ultimately, such work could help reduce the pace of biological aging and improve health and wellness.
本文旨在回顾近期关于创伤应激相关加速衰老的文献，重点关注细胞衰老的细胞机制和生物标志物以及加速生物衰老的临床表现。
多项研究表明，创伤后应激障碍（PTSD）与表观基因组、免疫和炎症系统的加速衰老有关，这可能反映在心脏代谢和心血管疾病的过早发生上。目前的研究状况为未来的工作铺平了道路，未来工作将聚焦于确定将创伤应激与加速生物衰老和医学发病联系起来的外周和中枢生物学机制，重点关注炎症、免疫功能、氧化应激、自主唤醒和应激反应所涉及的过程。最终，此类工作有助于减缓生物衰老速度，改善健康状况。
